Cardiovascular Disorders

A variety of cardiac disorders may lead to postural hypotension or even syncope. Pathologic processes such as mitral valve prolapse, aortic stenosis, or hypertrophic cardiomyopathy may limit cardiac output. Cardiac outflow may also be blocked in rare instances by a thrombus or myxoma when the patient is in the upright position. Certain paroxysmal cardiac dysrhythmias (bradycardias or tachycardias) may occur with activity or on standing and produce episodic hypotension or syncope; however, disturbances of cardiac rhythm are common in asymptomatic elderly persons, and their presence must be interpreted with caution. In patients with congestive heart failure, the heart rate and level of sympathetic tone may be such that compensatory adjustments cannot be made when the patient stands, and postural hypotension therefore results.

Alterations of Effective Blood Volume

Postural hypotension can occur because of loss of effective blood volume. Normal adults can withstand the loss of 500 ml of blood or bodily fluids with few if any symptoms, but greater volume depletion may occur acutely for a variety of reasons (e.g., hemorrhage or burns) and cause a postural drop in blood pressure. Hyponatremia and Addison disease may also lead to an absolute reduction in blood volume. Postural hypotension may occur owing to venous pooling in patients with severe varicose veins or congenital absence of venous valves or because of poor peripheral resistance and reduced muscle tone in patients with paralyzed limbs. Similarly, it may occur during the late stages of pregnancy owing to obstructed venous return by the gravid uterus. Marked vasodilatation, such as occurs in the heat or with the use of certain drugs or alcohol, sometimes causes postural hypotension.

Drugs

Numerous drugs may produce postural hypotension, including those given to treat neurologic disorders (e.g., dopamine agonists and levodopa) and psychiatric disturbances (e.g., tranquilizing, sedative, hypnotic, and antidepressant agents). Antihypertensive drugs, diuretics, and vasodilators commonly lead to postural hypotension as a side effect. Insulin may cause nonhypoglycemic postural hypotension in diabetic patients with autonomic neuropathy, possibly because of vasodilatation and reduced venous return in the absence of functioning compensatory mechanisms or because of impaired baroreceptor responses to changes in arterial pressure. Iatrogenic and toxic autonomic neuropathy is considered later.

Endocrine and Metabolic Disorders

Autonomic neuropathy, with consequent postural hypotension, is a major and common complication of diabetes. Postural hypotension may be a feature of Addison disease, hypopituitarism, myxedema, thyrotoxicosis, pheochromocytoma, carcinoid syndrome, and hypokalemia. It may also occur with anorexia nervosa. Anemia may exacerbate or cause postural hypotension.

Inadequate Postural Adjustments

Prolonged bed rest may result in postural hypotension when patients first begin standing again, but this problem is self-limited. Its cause is poorly understood, but it may be multifactorial. Carotid baroreceptor function is impaired, cardiac vagal activity is reduced, blood pooling is increased in the legs because of greater venous compliance, the total circulating blood volume and central venous pressure are reduced, and the red cell mass may decline. Prolonged bed rest also leads to an increased incidence of cardiac dysrhythmias. In otherwise healthy subjects, vigorous exercise to the point of exhaustion may also cause a postural decline in blood pressure, possibly because of marked peripheral vasodilatation and venous pooling.

Age

Many patients older than 70 years have a decline in systolic pressure of 20 mmHg or more on standing. Several causes of reduced orthostatic tolerance with advancing age have been identified. Baroreflex sensitivity declines with age and certain adrenoreceptors exhibit reduced sensitivity. Loss of preganglionic neurons also occurs with age and becomes symptomatic when approximately 50 percent of the cells are lost. Diuretics (which are commonly taken by the elderly) reduce blood volume and may lead to postural hypotension. Finally, structural, mechanical, and functional changes in the vascular system, such as loss of vascular elasticity and the occurrence of varicose veins, may be contributory, as may a reduction in the skeletal muscle mass. Prolonged bed rest, intercurrent illness, and adverse reactions to medication may also be important. Postural hypotension appears not to have an impact on mortality, at least among patients discharged from an acute geriatric ward.

Syncope is a common problem in the elderly. Often no precise explanation for it can be found, but postural hypotension is probably responsible in many instances. Nevertheless, it is best not to ascribe patients’ symptoms to postural hypotension unless they can be reproduced by a demonstrable fall in blood pressure on standing. Many of the homeostatic mechanisms that maintain intravascular volume and blood pressure may be impaired with advancing age, as discussed earlier, so that syncope is more likely to occur. Indeed, in many elderly patients a number of factors can be found to account for syncope, and it is then difficult to determine which of these factors is responsible in any individual instance.

Central Lesions and Spinal Injury

The autonomic consequences of spinal cord injuries depend on the level and severity of the lesion. In quadriplegic patients, the period of spinal shock that follows injury is associated with a dysautonomia in which the resting blood pressure and heart rate are typically low and postural hypotension is marked. This mandates that the patient be kept flat, without elevation of the head of the bed, and that any loss of blood volume be avoided or treated vigorously.

A few weeks after transection of the cervical cord, activity returns to the isolated spinal segment, but the brain is no longer able to control the sympathetic nervous system. Loss of regulation during postural change leads to orthostatic hypotension, whereas overactivity occurs if spinal sympathetic reflexes are activated and leads to the syndrome of autonomic hyperreflexia , which occurs in patients with cervical or high thoracic lesions. It is characterized by episodic hypertension, bradycardia, headache, and hyperhidrosis above the level of the lesion, with pallor and piloerection distal to it. Anxiety, confusion, nasal congestion, and facial flushing may also occur. Treatment of this syndrome thus requires avoidance of stimuli that activate spinal sympathetic reflexes (e.g., a distended bladder), elevation of the head of the bed, and, if necessary, use of short-acting antihypertensive agents such as calcium-channel blockers. In general, spinal cord transection produces postural hypotension if the lesion is above about the T6 level. Intramedullary and extramedullary tumors, transverse myelitis, and syringomyelia involving the cord above T6 may also produce dysautonomia.

A variety of brainstem lesions can impair autonomic function and affect control of the blood pressure, including syringobulbia and posterior fossa tumors. Chiari malformation with tonsillar herniation may lead to syncopal episodes. Impairment in Wernicke encephalopathy may relate to central or peripheral involvement. The extent to which autonomic reflex function, and particularly cardiovascular regulation, is impaired in Parkinson disease is disputed. Many patients with Parkinson disease have postural hypotension from cardiac (especially left ventricular) and extra-cardiac sympathetic denervation. In such patients, responses to the Valsalva maneuver are also abnormal. Other dysautonomic symptoms, such as disturbances of bladder or gastrointestinal function, and excessive salivation, are relatively common.

The findings in certain other disorders with parkinsonian features (e.g., multiple system atrophy, olivopontocerebellar atrophy, and striatonigral degeneration) are discussed on p. 153. Postural hypotension may also occur in diffuse Lewy body disease. Mild dysautonomic features may occur late in the course of progressive supranuclear palsy, but cardiovascular reflexes are usually preserved or show only minor abnormalities of dubious significance. A variety of dysautonomic symptoms may occur in Huntington disease, but any abnormalities of blood pressure regulation are usually mild and subclinical, except when related to neuroleptic medication taken for chorea or behavioral disturbances. Postural hypotension or other disturbances of cardiovascular autonomic function occur occasionally in patients with multiple sclerosis, but disturbances of bladder and bowel function are much more common dysautonomic features of that disorder. Wallenberg syndrome or bilateral brainstem strokes may lead to bradycardia and hypotension that may exacerbate the underlying neurologic problem.

Root and Peripheral Nerve Lesions

Postural hypotension may occur in patients with tabes dorsalis because of interruption of circulatory reflexes. In patients with polyneuropathies, autonomic involvement is not uncommon. It is particularly frequent in diabetic neuropathy, although usually relatively mild in severity ; indeed, diabetes is the most common cause of autonomic neuropathy in the more developed countries. Postural hypotension occurs in approximately 25 percent of patients with diabetic neuropathy. In addition to postural lightheadedness, the dysautonomia of diabetes may be manifest by impotence, postprandial bloating, early satiety, gastrointestinal motility disturbances, abnormalities of bladder control, and alterations of sweating. Cardiac vagal control is usually impaired early, before the development of postural hypotension; the quantitative sudomotor axon reflex test is commonly abnormal and indicates involvement of distal postganglionic sympathetic fibers.

Other polyneuropathies associated with postural hypotension include those of alcoholism, Guillain–Barré syndrome, malignant disease, idiopathic small-fiber neuropathies, and acute porphyria. In many patients with chronic alcoholism, however, there is no excessive decline in blood pressure on standing, although the cardiovascular responses to various maneuvers are often abnormal; both sympathetic and parasympathetic functions may be abnormal, and the presence of autonomic neuropathy has been correlated with nutritional status.

Primary amyloidosis and familial amyloid polyneuropathy of Portuguese type (FAP type 1) are often accompanied by dysautonomia consequent to the loss of predominantly unmyelinated and small myelinated peripheral fibers and of cells in the intermediolateral columns of the cord. Postural hypotension and impotence are early manifestations; episodic constipation and diarrhea, distal anhidrosis, impotence, urinary retention, and cardiac arrhythmias may also be conjoined. Tests of sympathetic and parasympathetic function are typically abnormal.

Autonomic dysfunction with abnormal cardiovascular responses occurs in some patients with chronic renal failure on intermittent hemodialysis, but the site of autonomic involvement is unclear. Vitamin B ₁₂ deficiency may lead to autonomic neuropathy and postural hypotension that improves or resolves completely after vitamin supplementation. Autonomic involvement, with impairment of sweating and cardiovascular responses, may occur in leprosy, sometimes without conspicuous features of peripheral nerve involvement. Symptoms of autonomic impairment, including postural hypotension, may be a presenting feature of systemic autoimmune disorders.

In Fabry disease, disturbed sweating, reduced saliva and tear production, impaired pupillary responses, and gastrointestinal symptoms are common, but postural hypotension does not usually occur, and postural cardiovascular reflexes are normal or only mildly abnormal.

Autonomic involvement in Guillain–Barré syndrome is usually mild, but paroxysmal cardiac arrhythmias or asystole or episodic hypertension may lead to a fatal outcome. Postural hypotension is common. It has a number of possible causes including inactivity and bed rest, baroreceptor deafferentation, efferent sympathetic denervation, hypovolemia, cardiac abnormalities, or some combination of these and other factors. The severity of autonomic involvement in Guillain–Barré syndrome is not related to the degree of sensory or motor disturbance, and a wide variety of autonomic abnormalities is found if patients are studied in detail. The hypertensive episodes may relate to catecholamine supersensitivity or denervation of baroreceptors. Treatment of Guillain–Barré syndrome is by supportive measures or with plasmapheresis or intravenous immunoglobulin therapy depending on disease severity. Patients with autonomic instability require close observation and management in an intensive care unit. Further aspects of treatment are given on p. 164. Curiously, postural hypotension is uncommon in chronic inflammatory demyelinating polyneuropathy, although mild impairment may be found in many patients on tests of autonomic function.

Autonomic neuropathy of acute or subacute onset, possibly on an autoimmune basis, sometimes occurs as a monophasic disorder in isolation or with associated sensory or motor involvement. It has occurred in the context of antecedent viral infections, malignancy, Hodgkin disease, infectious mononucleosis, ulcerative colitis, and certain connective tissue diseases. In approximately 50 percent of patients, high titers of ganglionic acetylcholine receptor (AChR) antibody are found. In patients with a paraneoplastic etiology, other autoantibodies may be present, including antineuronal nuclear antibody 1 (ANNA-1 or anti-Hu) or 2 (ANNA-2), Purkinje cell antibody 2 (PCA-2), and collapsin response-mediator protein 5 antibody (CRMP5). The presence of such antibodies may suggest the likely site of an underlying primary tumor. Both sympathetic and parasympathetic fibers are usually involved, leading to marked postural hypotension accompanied by a fixed heart rate, anhidrosis or hypohidrosis, heat intolerance, sphincter disturbances, gastroparesis, ileus, and dryness of the eyes and mouth, but occasionally abnormalities are confined to postganglionic cholinergic neurons (acute cholinergic neuropathy), in which case postural hypotension does not occur. Pure adrenergic neuropathy has also been described. Autonomic function tests reflect the clinical findings. Nerve conduction study results are typically normal, but sensory abnormalities are sometimes found. Treatment is supportive; immunomodulating therapy may have a role in those with severe disease. Paraneoplastic dysautonomia may remit if the underlying malignancy is treated. The prognosis of patients with acute or subacute autonomic neuropathies is guarded: approximately one-third of patients do well, but the remainder either fail to improve or are left with a major residual deficit, including marked postural hypotension.

Autonomic involvement may occur in a variety of hereditary polyneuropathies. In familial dysautonomia, or Riley–Day syndrome, many parts of the nervous system are affected. Presentation during infancy may be with inability to suck, but episodic vomiting, recurrent pulmonary infections, hypertension, tachycardia, and diaphoresis occur, especially after 3 years of age. There may also be emotional outbursts, difficulty in swallowing, hypothermia or hyperthermia, poor flow of tears, postural hypotension, and syncope. Sensory abnormalities include impaired pain and temperature appreciation, and the tendon reflexes are depressed. The tongue is smooth and lacks fungiform papillae. Cardiac arrest may occur on tracheal intubation. Treatment is essentially supportive. Postural hypotension usually is not a feature of the other hereditary sensory and autonomic neuropathies, whereas sudomotor function is often markedly impaired.

Autonomic symptoms or signs may occur in patients with hereditary motor and sensory neuropathy type 1, and abnormal vascular reflex responses may be present. Postural hypotension is usually not a conspicuous feature of the disorder.

Iatrogenic postural hypotension is common in the elderly and relates most often to the use of antihypertensive agents or diuretics. Iatrogenic polyneuropathies may be responsible in other instances, as reviewed elsewhere ; postural hypotension may be conspicuous in patients with the neuropathy caused by perhexiline maleate, cisplatin, paclitaxel (Taxol), vinca alkaloids, or amiodarone.

Toxic Exposure

Autonomic dysfunction may result from occupational or other exposure to certain neurotoxins but does not usually lead to postural hypotension. Long-term occupational exposure to a mixture of organic solvents may cause subtle disturbances of peripheral parasympathetic nerves as well as sensorimotor peripheral neuropathies, as reflected by cardiovascular reflex studies, but other reports of autonomic involvement in this context are few. Intentional inhalation of n -hexane or methyl- n -butyl-ketone for recreational purposes may lead to a rapidly progressive neuropathy with associated postural hypotension. Acrylamide neuropathy is usually accompanied by hyperhidrosis and cold, cyanotic extremities; experimental studies in animals reveal baroreceptor dysfunction, but the clinical significance of this in humans is unclear. A variety of autonomic symptoms (including tachycardia, hypertension, and disturbances of sweating) may occur with thallium, arsenic, or mercury poisoning, but postural hypotension is not usually a feature. The rodenticide N -3-pyridylmethyl- N ′- p -nitrophenyl urea (Vacor) has caused severe dysautonomia with disabling postural hypotension, as well as sensorimotor peripheral neuropathy and encephalopathic states. Symptoms reflecting autonomic dysfunction (anorexia, nausea, hyperhidrosis, and tachycardia) have been associated with cumulative exposure to moderate levels of pesticides, particularly organophosphate or organochlorine insecticides, regardless of recent exposure or history of poisoning, but specific comment was not made concerning symptoms of postural hypotension.

Primary Degeneration of the Autonomic Nervous System

Postural hypotension resulting from primary degeneration of the autonomic nervous system is well described. The postural hypotension is often exacerbated postprandially, and the normal circadian rhythm is reversed so that the blood pressure is highest at night and lowest in the morning. In addition, blood pressure typically declines with activity rather than increasing as in normal subjects. Other symptoms of dysautonomia in these patients include impotence, disturbances of bladder and bowel function, impaired thermoregulatory sweating, and xerostomia. Two distinct groups of patients are now recognized. In one, primary or pure autonomic failure leads to idiopathic orthostatic hypotension and other evidence of dysautonomia without peripheral neuropathy or CNS involvement. In the other, autonomic failure is associated with more widespread neurologic degeneration (i.e., with evidence of multiple system atrophy or MSA) such that there may be clinical features of parkinsonism or striatonigral degeneration (MSA-P), and often of more widespread neurologic lesions as well. A disorder similar to olivopontocerebellar atrophy may also occur (MSA-C). The autonomic deficit may precede the somatic neurologic one, or vice versa, but within a short period there is clinical evidence of both. Occasionally there is a family history of dysautonomia.

The time course and pattern of the dysautonomia reportedly differ between these two disorders. In pure autonomic failure, syncope and sudomotor dysfunction may precede the onset of constipation, bladder dysfunction, or respiratory disturbances whereas in multiple system atrophy, urinary complaints occur early and are then followed by abnormalities of sweating or by postural hypotension. Patients with pure autonomic failure had a slower functional deterioration and a better prognosis. The ingestion of water temporarily increases the seated blood pressure by uncertain mechanisms in patients with chronic autonomic failure. This occurs earlier in pure autonomic failure than multiple system atrophy, perhaps reflecting differing lesion sites in these two disorders.

In patients of both groups, plasma renin activity is usually subnormal. There are, however, a number of reported pharmacologic differences between them. Patients with pure autonomic failure have low plasma norepinephrine levels when lying down, and these levels fail to increase appropriately on standing; they also have a lower threshold for the pressor response to infused norepinephrine. The increase in plasma norepinephrine level in response to tyramine (see p. 161) is significantly less than in normal subjects or patients with multiple system atrophy. Extensive cell loss occurs in the intermediolateral cell columns of the thoracic cord, and the autonomic dysfunction has been attributed primarily to loss of these preganglionic sympathetic neurons. However, the pharmacologic studies described previously indicate that loss of postganglionic noradrenergic neurons also occurs, and norepinephrine may be depleted from sympathetic nerve endings.

By contrast, in multiple system atrophy, in which lesions are situated at multiple sites in the CNS, circulating norepinephrine levels are normal, suggesting that peripheral sympathetic neurons are intact, but plasma norepinephrine fails to increase appropriately with standing, implying that these neurons have not been activated. There is also an exaggerated pressor response to infused norepinephrine, but only patients with idiopathic orthostatic hypotension show a shift to the left in their dose–response curve, reflecting true adrenergic receptor supersensitivity.

Central catecholamine deficiency in these disorders is reflected by the levels in the cerebrospinal fluid of dihydroxyphenylacetic acid (a neuronal metabolite of dopamine), which are lower in patients with multiple system atrophy or pure autonomic failure than normal subjects, as also is dihydroxyphenylglycol, a metabolite of norepinephrine.

Endogenous arginine vasopressin is a powerful vasoconstrictor; it also acts on the kidney to control urinary concentrating mechanisms. The cardiovascular responses usually associated with arginine vasopressin are reduced cardiac output, heart rate, and plasma renin activity and increased vascular resistance and blood pressure. Arginine vasopressin helps maintain arterial pressure in certain hypotensive situations such as hemorrhage or volume depletion, but increased levels of arginine vasopressin do not normally affect the blood pressure significantly because the acute vasoconstrictor effects are buffered by the baroreceptor reflex. The chronic effects of vasopressin on renal function do not produce sustained retention of sodium and water, and so produce only minimal changes in mean arterial pressure.

Vasopressin release is influenced by the plasma’s osmotic pressure and by the activity of vascular stretch receptors. In normal people, plasma arginine vasopressin increases in response to standing, presumably because a decrease in venous return influences afferent activity from these stretch receptors. In patients with progressive autonomic failure or with multiple system atrophy, plasma levels similar to control values are found in the horizontal position, but the postural increase is markedly attenuated. A vulnerability has been suggested of the noradrenergic neurons of the caudal ventrolateral medulla that are involved in activating hypothalamic neurons involved in vasopressin secretion. However, in multiple system atrophy, loss of vasopressin neurons occurs in the posterior region of the hypothalamic paraventricular nucleus and may contribute to sympathetic failure, whereas loss of catecholaminergic input from the brainstem to the magnocellular vasopressin neurons may contribute to impaired vasopressin secretion following orthostatic stress.

Miscellaneous Disorders

Patients with Holmes–Adie syndrome may present with or develop postural hypotension or abnormalities of thermoregulatory sweating. Postural hypotension may occur in botulism ; however, blurred vision, dry mouth, and constipation are much more common autonomic manifestations. In rare instances, it relates to excessive amounts of endogenous bradykinin (a vasodilator) or a congenital defect of norepinephrine release. In patients with dopamine β-hydroxylase deficiency, norepinephrine and epinephrine cannot be synthesized, and dopamine is released from central and peripheral adrenergic nerve terminals. Severe postural hypotension is accompanied by other autonomic disturbances in association with absent norepinephrine and excessive dopamine levels in the plasma.

Orthostatic symptoms may develop in association with a significant tachycardia (an increase of 30 beats per minute or more or a heart rate of at least 120 beats per minute), but in the absence of consistent postural hypotension or an autonomic neuropathy. The designation postural orthostatic tachycardia syndrome (POTS) is applied to this disorder, which is more common in women than men and tends to occur in patients between 20 and 60 years of age. Symptoms on standing include tremulousness, lightheadedness, palpitations, visual disturbances, weakness, fatigue, anxiety, hyperventilation, nausea, postprandial bloating, and sweating, and may occur cyclically. Thus, orthostatic symptoms are accompanied by symptoms of sympathetic activation.

POTS can be associated with certain other disorders, especially joint hypermobility syndrome but also diabetes, paraneoplastic syndrome, amyloidosis, sarcoidosis, alcoholism, lupus, Sjögren syndrome, and heavy metal intoxication, and it may follow pregnancy, trauma, chemotherapy (especially with vinca alkaloids), or viral infections. It may also occur in association with mitral valve prolapse or a more specific dysautonomia. Its etiology remains uncertain. Proposed mechanisms include peripheral denervation, hypovolemia or a redistributed blood volume, prolonged deconditioning, β-receptor supersensitivity, psychologic mechanisms, and impaired brainstem regulation. Partial sympathetic denervation in the legs was suggested by studies of norepinephrine spill-over into the venous circulation of the limbs in response to various stimuli. There is impaired peripheral vasoconstriction on the Valsalva maneuver, but cardiovagal responses are normal. The optimal therapy for the disorder is not clear, but treatment may include volume repletion, a high salt diet and copious fluids, postural and psychophysiologic training, fludrocortisone, β-blocking agents, midodrine, serotonin reuptake inhibitors, and phenobarbital. Pyridostigmine is sometimes helpful, as also is methylphenidate.

General

Postural hypotension is usually the most disabling feature of autonomic failure. It leads to symptoms on or shortly after standing; they are relieved by sitting or lying down, and do not occur in the supine position. Such symptoms reflect cerebral hypoperfusion and include faintness, lightheadedness, blurred vision, and syncope. They may be particularly troublesome after exercise or a heavy meal (particularly a meal rich in carbohydrates) or in the morning when the blood pressure tends to be at its lowest (in contrast to healthy subjects). However, in some patients, marked postural hypotension may be clinically asymptomatic or may be accompanied by symptoms not usually regarded as suggestive of postural hypotension, such as nausea, breathlessness, heaviness or weakness of the limbs, episodic confusion, falling, staggering, headache and neck pain, and generalized weakness. Constipation may precipitate syncopal attacks during straining. Symptoms may also worsen in the heat because of vasodilatation and volume loss due to sweating. The symptoms of idiopathic POTS (discussed earlier) may be mistakenly attributed to postural hypotension, but occur without a significant decrease in blood pressure. Other causes, such as hypoglycemia, cardiac arrhythmias, or transient ischemic attacks, must be excluded if symptoms develop with the patient supine.

Impotence is a common initial symptom of autonomic dysfunction in men, often preceding other symptoms by several months or years. Bladder involvement may manifest by urinary frequency, urgency, incontinence, retention, and increased residual urine; urinary infections and renal calculi may occur in some patients with urinary stasis. Bowel dysfunction may lead to constipation, fecal incontinence, and diarrhea. Thermoregulatory sweating may be impaired. Pupillary abnormalities include Horner syndrome and anisocoria. Lacrimal dysfunction may lead to inadequate or excessive production of tears. Other symptoms of dysautonomia include night blindness, nasal congestion, and, sometimes, supine hypertension. Vocal abnormalities and respiratory disturbances (especially involuntary inspiratory gasps, cluster breathing, airway obstruction, and sleep apnea) sometimes occur, especially in patients with multiple system atrophy.

Syncope

Syncope refers to a sudden, transient loss of consciousness due to diffuse cerebral hypoperfusion or hypoxia. It is usually associated with flaccidity, but a generalized increase in muscle tone sometimes occurs with continuing cerebral ischemia/hypoxia, and there may be arrhythmic transient motor activity as well. Postictal confusion is usually brief (less than 30 seconds) when it occurs at all, unlike the marked postictal confusion that often follows a convulsion. Syncope has been divided into syncope from postural hypotension, reflex (i.e., neurally mediated) syncope, and cardiac syncope (arrhythmic or associated with structural cardiac disease).

Postural Change in Blood Pressure

In investigating patients with suspected autonomic dysfunction or postural hypotension, the blood pressure should be measured with the patient supine for at least 10 (preferably 20) minutes. The patient then stands up, and the blood pressure is measured again after 5 to 10 seconds, and again after 1, 2, and 5 minutes. There is normally an increase in pulse rate on standing, but the pulse rate may not change if there is already a high resting pulse or in patients with dysautonomia; furthermore, the change in heart rate may be blunted in the elderly. As for the blood pressure, there is normally a slight decline in systolic pressure, whereas diastolic pressure increases slightly. The response of the blood pressure is regarded as abnormal if systolic pressure decreases by at least 20 mmHg or diastolic pressure by 10 mmHg on standing. In some instances, postural hypotension develops only after exercise; it is therefore worthwhile to record the postactivity blood pressure if clinically feasible. It may be necessary to record the blood pressure on a number of occasions before the diagnosis of postural hypotension can be confirmed. In other instances, prolonged tilt (for up to 60 minutes) may be required to detect abnormalities.

The effect of postural change on blood pressure can be evaluated more accurately if the blood pressure is measured using an intra-arterial cannula or a noninvasive plethysmographic device with the patient resting quietly on a tilt-table; measurements are made continuously while the patient is supine and then at a 60-degree head-up tilt. The response to head-up tilt may differ from that obtained by standing because less enhancement occurs of the venous return to the heart by contraction of leg and abdominal muscles, and thus there is greater peripheral pooling of blood.

Blood pressure normally is higher in the day, declines at night, and rises prior to awakening. Patients with postural hypotension may show a circadian trend in blood pressure that is the reverse of normal subjects, with the highest pressures found at night and the lowest in the morning. Further, postural hypotension may be more severe in the morning after prolonged nocturnal recumbency due to a decline in stroke volume and cardiac output, resulting not only from nocturnal polyuria but also from a redistribution of body fluid. Such temporal variation in blood pressure implies that physiologic testing should be carried out at a standard time of day, especially if comparative studies are to be performed, and potentially harmful hypertension in response to treatment should be looked for especially during the early part of the night.

Postural Change in Heart Rate

A simple, noninvasive test of autonomic function consists of evaluating the response in heart rate to change from a recumbent to a standing position. There is typically a rapid increase in heart rate that is maximal at approximately the fifteenth beat after standing, with a subsequent slowing from the initial tachycardia (i.e., a relative bradycardia) that is maximal at approximately the thirtieth beat ( Fig. 8-3 ). This response is mediated by the vagus nerve. For testing purposes, the R-R interval at beats 15 and 30 after standing can be measured to give the 30/15 ratio, as reviewed in detail elsewhere. Values greater than 1.03 occur in normal subjects, whereas in diabetic patients with autonomic neuropathy (who typically show only a gradual increase in heart rate), values are 1.00 or less. Some prefer to measure the ratio of the absolute maximum to absolute minimum heart rate after standing, which may not coincide with the heart rates at beats 15 and 30. This test does not depend on the resting heart rate and correlates well with the Valsalva ratio and the beat-to-beat variation in heart rate, described later. Studies suggest that the value for the 30/15 ratio declines with age in normal subjects.

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