Orthostatic hypotension and supine hypertension in pure autonomic failure]

Orthostatic hypotension is associated with significant morbidity and mortality in elderly patients. In orthostatic hypotension caused by central and peripheral nervous system disorders (neurogenic orthostatic hypotension), the release of catecholamine in the standing posture is insufficient to compensate adequately for decreased venous return to the heart. Primary autonomic failure exhibits, often, supine hypertension, that can be worsened by pressor agents, such as midodrine, used to prevent syncope episodes. Salt-retaining steroid fludrocortisone, also, used to treat orthostatic hypotension, increases blood pressure both in supine and in standing position. We describe 3 patients with neurogenic orthostatic hypotension caused by pure autonomic failure. They complained of several syncope episodes. On examination, orthostatic hypotension and supine hypertension were detected in the absence of pharmacological therapy. All the patients presented hypertensive organ disease. Fludrocortisone acetate was started in one patient, and short-acting vasopressor agents during the day and dihydropyridine-calcium antagonist during the night in the other two. During the follow-up a transient ischemic attack occurred in the patient treated with fludrocortisone. When fludrocortisone was titrated down and short-acting antihypertensive drugs were started, the patient did not complain of any symptoms. Supine hypertension is part of pure autonomic failure, and short-acting antihypertensive agents should be associated with vasopressor agents to prevent hypertensive target organ disease.     

Association between supine hypertension and orthostatic hypotension in autonomic failure

Supine hypertension occurs commonly in primary chronic autonomic failure. This study explored whether supine hypertension in this setting is associated with orthostatic hypotension (OH), and if so, what mechanisms might underlie this association. Supine and upright blood pressures, hemodynamic responses to the Valsalva maneuver, baroreflex-cardiovagal gain, and plasma norepinephrine (NE) levels were measured in pure autonomic failure (PAF), multiple-system atrophy (MSA) with or without OH, and Parkinson's disease (PD) with or without OH. Controls included age-matched, healthy volunteers and patients with essential hypertension or those referred for dysautonomia. Baroreflex-cardiovagal gain was calculated from the relation between the interbeat interval and systolic pressure during the Valsalva maneuver. PAF, MSA with OH, and PD with OH all featured supine hypertension, which was equivalent in severity to that in essential hypertension, regardless of fludrocortisone treatment. Among patients with PD or MSA, those with OH had higher mean arterial pressure during supine rest (109+/-3 mm Hg) than did those lacking OH (96+/-3 mm Hg, P=0.002). Baroreflex-cardiovagal gain and orthostatic increments in plasma NE levels were markedly decreased in all 3 groups with OH. Among patients with PD or MSA, those with OH had much lower mean baroreflex-cardiovagal gain (0.74+/-0.10 ms/mm Hg) than did those lacking OH (3.13+/-0.72 ms/mm Hg, P=0.0002). In chronic autonomic failure, supine hypertension is linked to both OH and low baroreflex-cardiovagal gain [corrected]. The finding of lower plasma NE levels in patients with than without supine hypertension suggests involvement of pressor mechanisms independent of the sympathetic nervous system.     

Diagnosis and treatment of supine hypertension in autonomic failure patients with orthostatic hypotension

Orthostatic hypotension is seen in various medical conditions. It can be secondary to medications or volume depletion. It can also be due to autonomic neuropathy secondary to other diseases, such as diabetes mellitus, or to primary degenerative processes of the autonomic nervous system. Orthostatic hypotension dominates the clinical picture of patients suffering from autonomic failure. Paradoxically, about one half of these patients also suffer from supine hypertension, which induces pressure natriuresis, worsening orthostatic hypotension. It also complicates the treatment of orthostatic hypotension. Supine hypertension is mediated by an increase in peripheral vascular resistance. This is due to residual sympathetic tone in patients with multiple system atrophy (Shy-Drager syndrome), but the cause is not known in patients with pure autonomic failure, who have increased vascular resistance despite very low levels or plasma norepinephrine and renin activity. The recent observation that patients with supine hypertension develop left ventricular hypertrophy suggests they should be treated. During the day, avoiding the supine position is often all that is required. Short-acting vasodilators (e.g., transdermal nitroglycerin) can be used during the night.     

Orthostatic hypotension due to hypertrophic cardiomyopathy and autonomic failure

A case of orthostatic hypotension due to the combination of hypertrophic obstructive cardiomyopathy and autonomic failure is described. The interacting pathophysiologic features of the two disorders and response to therapy are discussed. The value of dynamic cardiac auscultation and Doppler echocardiography in patients with postural blood pressure changes is demonstrated.     

Orthostatic hypotension due to autonomic disorders in the hypertension clinic

Hypertension specialists are consulted regarding orthostatic hypotension (OH) or the combination of OH with supine hypertension. These clinical presentations are often associated with a variety of underlying autonomic disorders. A comprehensive medical history and clinical examination with attention to autonomic signs and the neurological system may suggest the possible etiology or a differential diagnosis. At times, drug therapy for hypertension or other diseases such as Parkinson's is temporally associated with the onset of OH. At other times, no definitive association can be made. Most hypertension specialists can initiate basic evaluation and treatment. Treatment approaches to OH must be targeted primarily to alleviate symptoms of cerebral hypoperfusion and also be cognizant of supine hypertension. Several lifestyle and drug therapies can ameliorate symptoms of OH. Short-acting antihypertensive therapy may be useful in controlling nocturnal supine hypertension.     

Orthostatic hypotension: pathophysiology,assessment, treatment and the paradox of supine hypertension

Both hypertension and orthostatic hypotension (OH) are strongly age‐associated and are common management problems in older people. However, unlike hypertension, management of OH has unique challenges with few well‐established treatments. Not infrequently, they both coexist, further compounding the management. This review provides comprehensive information on OH, including pathophysiology, diagnostic workup and treatment, with a view to provide a practical guide to its management. Special references are made to patients with supine hypertension and postprandial hypotension and older hypertensive patients.     

Clonidine for the treatment of supine hypertension and pressure natriuresis in autonomic failure

Patients with autonomic failure are disabled by orthostatic hypotension, which can be worsened by the nighttime pressure natriuresis induced by associated supine hypertension. Several pharmacological agents are available that effectively reduce nighttime hypertension, but none of them prevent pressure natriuresis. Because hypertension of autonomic failure can be driven by residual sympathetic tone, we hypothesized that clonidine would be effective in reducing blood pressure (BP) and nocturnal natriuresis. Therefore, we determined the effect of placebo, 0.1 mg clonidine, and 0.1-mg/h nitroglycerin transdermal patch on supine BP, orthostatic hypotension, and pressure natriuresis in 23 patients with primary autonomic failure and supine hypertension. Medications were given at 8:00 PM, and BP was recorded every 2 hours for 12 hours. The maximal decrease in BP was seen 6 to 8 hours after drug administration and was similar to clonidine and nitroglycerin (-29+/-9 and -30+/-10 mm Hg, respectively), as was the average fall in BP throughout the night. However, only clonidine effectively reduced nocturnal natriuresis (-0.09 mmol/mg Cr; 95% CI, -0.13 to -0.04; P=0.004), but this was not associated with improvement in morning orthostatic hypotension because of a residual hypotensive effect. The decrease in BP induced by clonidine was modestly but significantly correlated with the magnitude of residual sympathetic tone determined in 10 subjects by the fall in BP induced by ganglionic blockade (r=0.66; P=0.043). These results are consistent with residual sympathetic tone contributing to supine hypertension in autonomic failure, which can be targeted with clonidine to decrease BP and nocturnal natriuresis.     

Orthostatic hypotension in elderly women with congestive heart failure

Orthostatic hypotension is common in the elderly and could be the cause of impaired vision, dizziness, fainting spells and falls. To date, studies on orthostatic hypotension have chiefly concentrated on elderly patients in nursing homes, outpatients or healthy subjects. Congestive heart failure (CHF) is one of the most common causes of hospitalization and pharmacotherapy in the elderly, but little is known about the orthostatic hypotension in patients with CHF. The aim of this study was to evaluate the prevalence of orthostatic hypotension and associated symptoms in elderly females hospitalized for CHF. The study group included 36 women aged 70-100 years (mean 82.2), admitted to hospital for congestive heart failure. The control group consisted of 15 women aged 71-95 years (mean 82.5) with no symptoms of heart failure or other diseases, who underwent earlier epidemiological studies on Cracow's elderly population. In all subjects a tilt test was performed (60 degree tilt for 10 minutes) under standardized conditions (fasting patients, 12 hours after the last administration of medications, between 8:00 and 10:00 a.m.). Orthostatic hypotension was defined as a decline of 20 mmHg or more in systolic blood pressure, or 10 mmHg or more in diastolic blood pressure on assumption of the upright position. Orthostatic hypotension was detected in 83.3% of CHF women, and 43.3% of them manifested clinical symptoms associated with it. In the control group, orthostatic hypotension was noted in 53.3% of women, but none was symptomatic. In particular, the CHF patients showed a decreased ability to develop compensatory tachycardia during hypotension. Moreover, reduction in systolic blood pressure was more pronounced in CHF patients, and diastolic blood pressure increase was less significant as compared with the control group.     

Orthostatic hypotension

A common problem among elderly people, orthostatic hypotension is associated with significant morbidity and mortality, which may be caused by medications, the cumulative effects of age- and hypertension-related alterations in blood pressure regulation, or age-associated diseases that impair autonomic function. Evaluation requires multiple blood pressure measurements taken at different times of the day and after meals or medications. Central and peripheral nervous system disorders should be sought, and the laboratory evaluation should concentrate on ruling out diabetes mellitus, amyloidosis, occult malignancy, and vitamin deficiencies. If orthostatic hypotension is detected, it should be considered a risk factor for adverse outcomes and treated first with nonpharmacologic interventions, including the withdrawal of potentially hypotensive medications. In patients with hypertension and orthostatic hypotension, the judicious treatment of hypertension may be helpful. For persistent, symptomatic orthostatic hypotension caused by autonomic failure, pharmacologic interventions include fludrocortisone, midodrine, and a variety of other agents. The careful evaluation and management of orthostatic hypotension will hopefully result in a significant reduction in falls, syncope, and fractures, and an attenuation of functional decline in elderly patients.     

Orthostatic hypotension in pediatrics

Transient orthostatic hypotension is a common experience of many healthy adolescents and is the expected outcome of relatively dilated-dependent vascular tone. These children may experience brief symptoms of orthostatic intolerance when standing up rapidly, but they have no chronic symptoms or diseases. However, persistent orthostatic hypotension and chronic symptoms of orthostatic intolerance indicate postural tachycardia syndrome.     

Orthostatic hypotension. A primary care primer for assessment and treatment

Orthostatic hypotension (OH), defined as a decline in blood pressure when a person moves from a supine to sitting or standing position, is a common physical finding in the primary care setting. It is associated with several medical conditions and its prevalence increases with age. Treatment is specific to cause. Drug-induced OH often can be alleviated by reducing dosage or completely changing medications. OH secondary to autonomic insufficiency or neurogenic causes remains a challenge to manage, and a combination of non-pharmacologic and pharmacologic measures are needed. Recommendations are made for preventive measures, patient and caregiver education, and nonpharmacologic and pharmacologic approaches to treatment. Approaches to managing OH in conjunction with hypertension are also discussed.