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PubMed1990

[New viewpoints on the clinical picture, diagnosis and pathophysiology of reflex sympathetic dystrophy (Sudeck's disease)].

Reflex sympathetic dystrophy can be elicited by various factors (e. g. trauma, herpes zoster, myocardial infarction). Independent of kind and site of a lesion, symptoms occur most often in the whole distal part of the affected extremity. There in most cases, a triad of autonomic, motor and sensory disturbances can be found clinically. For early diagnosis--beside clinical investigation--a comparative measurement of skin temperatures on both sides of finger or toe tips, respectively, is recommended. Hereby the clinical finding of a warmer or colder extremity can be proved, which supplies evidence of a disturbed skin blood flow. In case, the above mentioned triad and a disturbance of skin circulation is found, diagnosis of sympathetic reflex dystrophy can be made with great certainty. With regard to the underlying pathophysiology, symptoms can be explained at this time satisfactory only by the assumption of a vicious circle. Starting from a painful event (e.g. trauma, mark in a plaster cast, nerve lesion or myocardial infarction) a functional disturbance of the sympathetic nervous system is initiated. This results in a disturbance of the circulation in all of the affected tissues (skin, muscle, bone and joint), which finally gives rise to an abnormal excitation of afferent receptors, particularly of nociceptors. This excitation maintains the disturbance of the sympathetic nervous system at central nervous level (vicious circle). The most relevant pathomechanism in this process seems to be the occurrence of an imbalance between the activity of sympathetic vasoconstrictor neurons supplying arteries and those, supplying veins. A sympatholytic therapy, if applied in time, is able to cut off the vicious circle, which may lead to a restitutio ad integrum. Further investigations will show to what extent psychological factors are involved in developing the central nervous disturbance of the sympathetic nervous system and may also show if in addition the motor system is affected.

Diagnosis, Differential↗

PubMed2003

[Sympathetic overactivity and the kidney].

Hypertension is present in the majority of patients with chronic renal failure and constitutes a major risk factor for the very high cardiovascular morbidity and mortality in this patient population. Furthermore hypertension is known to be a substantial progression factor in renal disease. In the past, it had been presumed that hypertension in chronic renal failure is due to enhanced sodium retention, chronic hypervolemia and increased activity of the renin-angiotensin-aldosterone-system. Recent studies now provide evidence that sympathetic overactivity plays an additional important role and also promotes progression of renal failure. The treatment goal in renal patients is to delay or even prevent progression of renal failure and to reduce the cardiovascular risk. Recent studies have investigated the respective impact of sympatholytic drugs, e.g. inhibitors of the renin-angiotensin-aldosterone-system, beta-blockers or I1-Imidazolin-receptor-agonists in fulfilling these aims. The present report will review experimental and clinical studies on the role of sympathetic overactivity in hypertension and chronic renal failure and possible new therapeutic options.

Animals↗

PubMed1997

Comparison of the effects of high ambient temperature and clonidine on autonomic functions in man.

The effects of two interventions, high ambient temperature, a sympathetic activator, and clonidine, a centrally acting sympatholytic drug, were compared on a number of autonomic functions. Eight healthy male volunteers participated in four weekly sessions. Each session was associated with one of the following treatments: placebo (physiological saline infused intravenously over 10 min) at 20 degrees C; clonidine hydrochloride (1.5 micrograms kg-1 in 10 ml infused intravenously over 10 min) at 20 degrees C; placebo at 40 degrees C; clonidine at 40 degrees C. Subjects were allocated to treatments and sessions according to a double-blind (for drug condition) balanced design. In each session, the following indices of autonomic function were recorded: systolic and diastolic blood pressure, heart rate, salivation, body temperature, plasma noradrenaline and adrenaline concentrations, baseline and carbachol-evoked sweating, physiological finger tremor. Raised ambient temperature (40 degrees C) caused increases in heart rate, body temperature, carbachol-evoked sweating and physiological finger tremor. Clonidine (at 20 degrees C) reduced systolic blood pressure, body temperature, salivation and plasma noradrenaline concentration, but did not affect any of the other measures. Clonidine (at 40 degrees C) counteracted the increase in heart rate, but not the increases in carbachol-evoked sweating and finger tremor, evoked by high ambient temperature. The high ambient temperature condition abolished the body-temperature-lowering effect of clonidine, but did not modify the effects of clonidine on systolic blood pressure, salivation and plasma noradrenaline concentration. These result indicate that while the effects of the heat stressor are consistent with an increase in sympathetic activity, and most of the effects of clonidine are consistent with a decrease in sympathetic activity, only two functions (body temperature and heart rate) were affected in opposite directions by the two interventions. Indeed physiological antagonism between the two interventions could be demonstrated on body temperature and heart rate only, and there was no evidence for an interaction between the effects of the two variables on any of the other indices of autonomic activity. The failure of clonidine to affect two sympathetically mediated functions, carbachol-evoked sweating and physiological finger tremor, under either temperature condition, indicates that central alpha 2-adrenoceptors cannot be involved in the regulation of these functions.

Adrenergic alpha-Agonists↗

PubMed1994

[Endocrine stress reaction, hemodynamics and recovery in total intravenous and inhalation anesthesia. Propofol versus isoflurane].

This prospective, randomised study compared total intravenous anaesthesia (TIVA) and inhalation anaesthesia with respect to endocrine stress response, haemodynamic reactions, and recovery. METHODS. The investigation included two groups of 20 ASA I-II patients 18-60 years of age scheduled for orthopaedic surgery. For premedication of both groups, 0.1 mg/kg midazolam was injected IM. Patients in the propofol group received TIVA (CPPV, PEEP 5 mbar, air with oxygen FiO2 33%) with propofol (2 mg/kg for induction followed by an infusion of 12-6 mg/kg.h) and fentanyl (0.1 mg before intubation, total dose 0.005 mg/kg before surgery, repetition doses 0.1 mg). For induction of patients in the isoflurane-group, 5 mg/kg thiopentone and 0.1 mg fentanyl was administered. Inhalation anaesthesia was maintained with 1.2-2.4 vol.% isoflurane in nitrous oxide and oxygen at a ratio of 2:1 (CPPV, PEEP 5 mbar). For intubation of both groups, 2 mg vecuronium and 1.5 mg/kg suxamethonium were injected, followed by a total dose of 0.1 mg/kg vecuronium. Blood samples were taken through a central venous line at eight time points from before induction until 60 min after extubation for analysis of adrenaline, noradrenaline (by HPLC/ECD), antidiuretic hormone (ADH), adrenocorticotropic hormone (ACTH), and cortisol (by RIA). In addition, systolic arterial pressure (SAP) heart rate (HR), arterial oxygen saturation (SpO2), and recovery from anaesthesia were observed. RESULTS. Group mean values are reported; biometric data from both collectives were comparable (Table 1). Plasma levels of adrenaline (52 vs. 79 pg/ml), noradrenaline 146 vs. 217 pg/ml), and cortisol (82 vs. 165 ng/ml) were significantly lower in the propofol group (Table 2, Figs. 1 and 3). Plasma levels of ADH (4.8 vs. 6.1 pg/ml) and ACTH (20 vs. 28 pg/ml) did not differ between the groups (Table 2, Figs 2 and 3). SAP (128 vs. 131 mmHg) was comparable in both groups, HR (68/min vs. 83/min) was significantly lower in the propofol group, and SpO2 (97.1 vs 97.4%) showed no significant difference (Table 3). Recovery from anaesthesia was slightly faster in the propofol group (following of simple orders 1.9 vs. 2.4 min, orientation with respect to person 2.4 vs. 3.4 min, orientation with respect to time and space 2.8 vs. 3.7 min), but differences failed to reach statistical significance. CONCLUSIONS. When compared with isoflurane inhalation anaesthesia, moderation of the endocrine stress response was significantly improved during and after TIVA with propofol and fentanyl. Slightly shorter recovery times did not lead to an increased stress response. With respect to intra- and postoperative stress reduction, significant attenuation of sympatho-adrenergic reaction comparable SAP and reduced HR, sympatholytic and hypodynamic anaesthesia with propofol and fentanyl seems to be advantageous for patients with cardiovascular and metabolic disorders. For this aim, careful induction and application of individual doses is essential.

Adolescent↗

PubMed2001

Influence of postoperative epidural analgesia with bupivacaine on intestinal motility, transit time, and anastomotic healing.

Epidural application of bupivacaine has been suggested to have a sympatholytic effect on spinal reflex mechanisms that shortens postoperative paralysis and leads to an improved transit time. The influence on anastomitic healing remains controversial. Laparotomy was performed in eight dogs. A short segment of the distal colon was resected and five electrodes were fixed on the serosa to measure the myoelectric activity (e.g., Migrating Myoelectric Complex--MMC). After operation a peridural catheter was placed between L7 and the sacral crest. One milliliter of bupivacaine 0.25% for each 3 kg of body weight was injected every 4 hours. Barium pellets coated in wax were placed into the stomach to allow radiographic representation of transit time. After 5 days the colon anastomosis was resected to measure the bursting pressure. In the peridural analgesia group (PDA) we found one small bowel intussusception and one covered anastomotic leakage. Postoperative PDA led to early and severe myoelectric activity but did not influence the time until the first MMC occurred (44 +/- 0.8 h, PDA; 44.6 +/- 1.5 h,control). Neither the transit time to the colon (50.2 +/- 1.9h, PDA; 51.7 +/- 5.5 h, control) nor the anastomotic healing was influenced (bursting pressure: 176 +/- 21.1 mmHg, PDA; 152 +/- 27.7 mmHg, control). Postoperative epidural analgesia with bupivacaine shortens intestinal paralysis. Early myoelectric activity with a lack of propulsive activity can cause complications like small bowel intussusception. Hence early postoperative enteral nutrition after epidural analgesia is risky. Because the influence of epidural analgesia on propulsive motility remains unclear, it seems reasonable to recommend its limited use in colon surgery.

Analgesia, Epidural↗

PubMed1998

[Cardiac sympathetic nerve activity in ischemic heart failure].

The prognosis in patients with heart failure, independent of etiology, is determined mainly by the extent of sympatho-adrenergic stimulation. In the development of heart failure sympathetic cardiac stimulation precedes systemic sympatho-adrenergic activation. Increased concentrations of the neurotransmitter norepinephrine can be found in the myocardium. This is a result of both increased release from sympathetic nerves as well as reduced neuronal reuptake. We were able to show that in advanced heart failure these effects are distributed heterogeneously in the heart. It has been shown experimentally that the effects on sympathetic neurotransmission are similar for both ischemia and heart failure. Therefore, these findings could indicate an important role of sympatholytic measures in patients with ischemia induced heart failure.

Heart↗

PubMed1997

[Acupuncture and reflex sympathetic dystrophy].

The term "reflex sympathetic dystrophy" (RSD) is used for various syndromes, e.g. posttraumatic edema, shoulder-hand syndrome, algodystrophy and causalgia. The clinical symptoms of RSD are characterized by a triad of autonomic, sensory and motor disturbances, which usually develop in the distal region of an affected extremity. The main symptoms are swelling, a side difference in skin temperature (autonomic symptoms), reduced active movements and muscular strength (motor symptoms) and spontaneous, deep, diffuse pain with an orthostatic component (sensory system). As soon as possible the treatment of RSD should include sympatholytic strategies and obligatory physical therapy. Acupuncture has also been reported to reduce sympathetic activity. The analgesic effect of acupuncture is well known, and therefore from an at least theoretical point of view, it should make sense to use acupuncture in the treatment of RSD. To date, however, no prospective, randomized, controlled, clinical long-term studies have been done. One short-term study showed promising results, but did not reach statistical significance. In that study acupuncture treatment seemed to alleviate the major symptoms of RSD. Since acupuncture rarely has side effects, its role as an additional option in the treatment of RSD should be further investigated.

English Abstract↗

PubMed1998

Concomitant aortic and renal artery reconstruction in patients on an intensive antihypertensive medical regimen: long-term outcome.

A beneficial effect in blood pressure control is presumed for patients on an intensive preoperative antihypertensive regimen who undergo empiric renal revascularization. Nonetheless, a noticeable decline in surgical cure rates for hypertension has been recently observed in patients with generalized atherosclerosis. The outcome of patients on multiple preoperative antihypertensive agents who underwent combined aortic and renal artery reconstruction was reviewed. The study population comprised 43 patients who underwent concomitant renal artery and aortic reconstruction for atherosclerotic disease between 1983 and 1995 and who were taking two or more antihypertensive medications and had a serum creatinine of less than or equal to 1.7 mg/dL. Operative management included an aortic reconstruction with either unilateral (n = 22) or bilateral (n = 19) aortorenal bypass or renal endarterectomy (n = 2). Operative mortality was 4.7% (2 of 43). The estimated 5-yr probability of survival was 83% (95% C.I. 0.70, 0.99). Late follow-up data on blood pressure control were available for review in 32 patients at a median follow-up of 37 months. Hypertension was cured in 1 (3%) and improved in an additional 15 (47%) patients. The numbers of antihypertensive medications taken preoperatively (mean = 2.7) declined at late follow-up (mean = 1.6). Notably, the largest reduction was observed with beta blockers (p = 0.006), central sympatholytics (p = 0.041), and angiotensin converting enzyme (ACE) inhibitors (p = 0.052). The number of preoperative antihypertensive medications was not significantly related to survival or to blood pressure improvement. However, uncontrolled preoperative hypertension despite antihypertensive therapy was associated with a favorable blood pressure response to operation (p < 0.001). Patients on an intensive antihypertensive regimen can safely undergo concomitant renal artery and aortic reconstruction for the empiric management of hypertension. Poorly controlled preoperative hypertension in the presence of multiple antihypertensive agents is a favorable marker for improved postoperative blood pressure control.

Aged↗

PubMed2004

Effects of nitroglycerin treatment on cardiac autonomic control in heart failure.

There is substantial animal data suggesting that nitric oxide (NO) has an important role as a modulator of cardiac autonomic control with a net vagotonic and sympatholytic role. Recent human work would support this concept. This study investigated the effects of the NO donor glyceryl trinitrate (GTN) upon measures of cardiac vagal activity in heart failure. Twelve stable chronic heart failure patients were studied in a randomised double blind, placebo controlled crossover study to assess the effects of chronic treatment with transdermal GTN (10 mg per day) on heart rate variability (HRV) measures of cardiac vagal activity. No significant difference between GTN and placebo was observed in mean arterial blood pressure and most measures of HRV and baroreflex sensitivity (BRS). BRS measured by the alpha-LF index showed a small rise. In conclusion, chronic GTN administration does not produce a significant increase in HRV measures of cardiac vagal activity in patients with heart failure.

Administration, Cutaneous↗

PubMed2005

Clonidine lowers blood pressure by reducing vascular resistance and cardiac output in young, healthy males.

PURPOSE: Clonidine is a classical sympatholytic drug that is widely used for the treatment of hypertension. Experimental and clinical studies suggest that Clonidine may activate baroreflex. The aim of this study was to determine the hemodynamic response to Clonidine under physiological conditions and to test the hypothesis that Clonidine would reduce cardiac output and blood pressure resulting in an increase in total peripheral resistance. METHODS: Clonidine's hemodynamic effect was evaluated in 28 young, healthy subjects after a single i.v. dose of 1 microg x kg(- 1). Impedance cardiography, systolic time intervals and pulse wave analysis were used to characterize myocardial and vascular function. RESULTS: Clonidine lowered blood pressure, heart rate, left ventricular ejection time, and pulse wave velocity and increased pre-ejection period. Stroke volume and cardiac output decreased gradually over the investigation time of 240 min. Central systolic blood pressure (SBP) was lowered to a larger extent than peripheral SBP. Total peripheral resistance was characterized by an immediate fall of short duration followed by a continuous rise above baseline after 120 min. Placebo did not have any significant effect on hemodynamic parameters. CONCLUSIONS: Clonidine's blood pressure lowering effect is mediated by both an immediate decrease in vascular resistance and a prolonged decrease in cardiac output, and Clonidine lowers central SBP more than peripheral SBP.

Adult↗

PubMed2002

Effects of antihypertensive therapy on sexual activity in hypertensive men.

Sexual dysfunction has a high prevalence among hypertensive men, and hypertension per se, regardless of drugs, has been suggested to affect sexual function. The available studies have not clarified which factors play a major role in the pathogenesis of sexual dysfunction in hypertensive men. Neurovascular factors, however, seem to be especially important, (in particular defective nitric oxide activity), although hormonal and psychogenic factors cannot be excluded. Further studies are needed to answer the important question of whether erectile dysfunction seen in hypertension may be one expression of vascular disease and target organ damage. The incidence of sexual dysfunction is exacerbated by antihypertensive drug treatment. There is evidence that some classes of drugs, such as diuretics, centrally acting sympatholytic drugs, and b-blockers have a greater impact on sexual function than other classes, such as calcium antagonists and angiotensin converting enzyme inhibitors. Present evidence on the effects of angiotensin II antagonists is limited, but some data suggest that sexual function in men receiving these drugs not only is not altered, but even improves. Since sexual function is an important aspect of quality of life for the individual, it is important in treating hypertension to ensure that the drugs used have the lowest possible potential for causing sexual problems. This ensures the best balance between therapeutic efficacy and quality of life, which is essential for compliance.

Antihypertensive Agents↗

PubMed2000

Raynaud's Phenomenon.

Raynaud's phenomenon may be primary (idiopathic) or secondary. Primary Raynaud's phenomenon is very common in young women, especially in cool climates. Treatment of patients with primary disease is usually much more successful than treatment of patients with secondary disease. Most patients respond to conservative measures. Reassurance that they will not lose digits or limbs is helpful. They should avoid instigating vasospastic attacks, which are usually caused by cold plus pressure on the digits. Reflex sympathetic vasoconstriction can be avoided by wearing warm clothing, including hats. Mittens are more protective than gloves, which separate the fingers. Many patients find chemical hand and foot warmers very useful. Pavlovian conditioning and biofeedback may be helpful if the patient is willing to spend the time. Underlying disease should be treated or instigating causes avoided in secondary Raynaud's phenomenon. In the more severe cases of primary Raynaud's phenomenon as well as in secondary cases, drug therapy is often beneficial. Calcium entry blockers have yielded the best results. Forms of nifedipine with extended action should be prescribed; felodipine or isradipine can be tried if nifedipine cannot be tolerated owing to frequent side effects. When these drugs fail or are not tolerated, sympatholytic drugs (eg, prazosin, reserpine, guanethidine) have benefited some patients. We have not found nitroglycerin preparations to be of benefit. In severe digital ischemia that does not respond to drug therapy, digital artery sympathectomy may help heal digital ulcers. Cervicodorsal sympathectomy is not recommended for upper extremity symptoms, but lumbosacral sympathectomy will often cure vasospastic attacks of the toes.

Journal Article↗

PubMed2006

Management of hypertension in the setting of autonomic dysfunction.

Supine hypertension is a common finding in patients with autonomic failure; it is associated with end-organ damage and produces nighttime pressure diuresis with worsening of orthostatic hypotension. During the daytime, it is best treated by avoiding the supine posture. At night, simple measures such as raising the head of the bed by 6 to 9 inches can be effective, but most patients require pharmacologic treatment. Transdermal nitroglycerin (0.1 to 0.2 mg/h) or nifedipine (30 mg, orally) has proved to be effective. Hydralazine and minoxidil are usually less effective but may be useful in a given patient. One key therapeutic concept is the hypersensitivity of these patients to depressor agents, requiring a careful titration of the doses on an individual basis. For those patients with proven residual sympathetic tone, as in multiple system atrophy, central sympatholytics such as clonidine may provide an alternative.

Journal Article↗

PubMed1982

Evaluation of the chronotropic property of captopril in hypertensive patients.

Captopril was administered (50 mg orally) to 88 untreated hypertensive patients (70 with essential hypertension, eight with renal arterial disease, 10 with renal parenchymal disease) and to 25 hypertensive patients treated with sympatholytic or beta-blocking agent (20 with essential hypertension, five with renal arterial disease). In the former group, captopril caused a decrease in heart rate (HR) in 18 patients and an increase in only two. As a whole, captopril caused significant decreases in blood pressure without increase in HR. Significant negative correlation was observed between change in HR and plasma renin activity obtained before captopril administration (n = 79, r = -0.425, p less than 0.0001). Hypotensive and chronotropic effects of captopril were almost identical in untreated and treated patients. Hypotensive effects caused by captopril and nifedipine (20 mg orally) were almost identical. Nifedipine caused reflex tachycardia, while captopril caused slight bradycardia. Absence of compensatory tachycardia appears to be related to reduction of endogenous angiotensin II by captopril.U

Adrenergic beta-Antagonists↗

PubMed1985

The effect of bretylium and clofilium on dispersion of refractoriness and vulnerability to ventricular fibrillation in the ischemic feline heart.

Bretylium has been shown to have a pronounced antifibrillatory effect. The purpose of this study was to examine the effects of bretylium on changes in vulnerability to ventricular fibrillation (VF) and refractoriness which occur during acute myocardial infarction. Right ventricular VF thresholds and effective refractory periods (ERP) at six left ventricular sites were measured before and serially after left anterior descending coronary occlusion in chloralose-anesthetized cats. In eight untreated animals, there was a decrease in VF thresholds of 73% (p less than 0.01) immediately after occlusion and dispersion of refractoriness (DR) (maximum difference in ERP between normal and ischemic left ventricular sites) increased from 18 +/- 4 to 50 +/- 6 msec (p less than 0.01). Five of eight animals manifested spontaneous VF within the first minutes of occlusion but none had nonsustained VF. Pretreatment with bretylium (10 to 20 mg/kg intravenously) increased resting ERP from 181 +/- 9 to 201 +/- 9 msec (p less than 0.05) and VF threshold from 32 +/- 5 to 85 +/- 7 mA (p less than 0.001). Bretylium also prevented spontaneous VF in all eight animals and abolished occlusion-related changes in VF and DR. Fourteen animals were similarly studied using clofilium, a bretylium congener which is devoid of sympatholytic effect (no effect on blood pressure response to bilateral carotid artery occlusion). Clofilium increased resting ERP and VF thresholds at both low (0.5 mg/kg intravenously) and high doses (5 mg/kg intravenously). High-but not low-dose clofilium blunted the fall in VF threshold after coronary occlusion. In addition, DR correlated with VF threshold changes at both doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Hemodynamic response patterns to mental stress: diagnostic and therapeutic implications.

Stress has been identified as contributing to the development of cardiovascular disease. The pathophysiologic link between stress and disease still remains unclear. Because experimental stress testing in the laboratory permits the examination of the underlying mechanism for stress-induced blood pressure, analyses of cardiovascular reactivity during emotional stress could be of particular clinical importance. The analyses of pooled data during the past 6 years (n = 298, age from 20 to 60 years, normotensive subjects as well as patients with borderline and mild essential hypertension) reveal that stress-induced changes in stroke volume and especially in total peripheral resistance are crucial parameters to analyze the hemodynamic stress response. However, neither those simple nor complex response patterns such as "hot reactor" describe clinically distinct subgroups of persons. When physiologic testing was repeated in hypertensive patients after effective long-term antihypertensive therapy with clonidine, oxprenolol, nitrendipine, or enalapril, no attenuation of the stress-induced increase in blood pressure was found in any of these groups. However, heart rate reactivity and stress-induced changes in total peripheral resistance were altered significantly by oxprenolol and nitrendipine. The beta-adrenoceptor blocker decreased heart rate reactivity and increased reactivity of peripheral resistance; the calcium antagonist decreased stress-induced changes in peripheral resistance and increased the heart rate response. The centrally acting sympatholytic regimen and the angiotensin-converting enzyme inhibitor had no impact on the hemodynamic response pattern during emotional challenge.

Adult↗

PubMed1982

Comparative effects of captopril and MK 421 on sympathetic function in spontaneously hypertensive rats.

The effects of captopril and MK 421, both orally active angiotensin-converting enzyme inhibitors, on sympathetic function in the pithed spontaneously hypertensive rats were examined. Captopril (100 mg/kg orally) significantly inhibited pressor responses to sympathetic nerve stimulation and norepinephrine whereas MK 421 (10 and 100 mg/kg orally) was without effect. Both drugs abolished the angiotensin I response without affecting that to angiotensin II. Because these doses of MK 421 are antihypertensive in the spontaneously hypertensive rat, it is concluded that inhibition of sympathetic function plays no role in its effect. The role of the sympatholytic action of captopril in its antihypertensive action remains unclear.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1983

Pathophysiologic considerations in the treatment of the elderly hypertensive patient.

Changes that occur as a consequence of aging can influence the development of hypertension and its complications. Such changes may adversely affect cardiac function and tissue blood flow and the responsiveness of the circulation to antihypertensive therapy. The distribution and metabolism of antihypertensive drugs may also be influenced by aging. These factors can complicate the pharmacologic management of the elderly hypertensive patient and may lead to a higher incidence of side effects. A conservative approach to the treatment of isolated systolic hypertension is indicated because the merits of therapy remain uncertain. Although standard stepped-care treatment can be used, certain special precautions should be considered. Lower doses of medications are generally required in elderly than in young hypertensives. Hypokalemia and volume contraction are the more frequent and more clinically important complications of diuretic therapy, while sluggishness, sexual dysfunction, or decreased mentation are more commonly observed with sympatholytic agents. Complications from beta-adrenergic blockers also are relatively frequent in elderly persons. Calcium-channel blockers, although not approved in the United States for the treatment of hypertension, may be beneficial in these patients. When diastolic hypertension is also present, a vigorous approach to lowering blood pressure should be used because the benefits of such therapy have been well documented. However, similar precautions should be used in these patients as in those with systolic hypertension.

Aged↗