Printer Friendly

Recognition and Management of Orthostatic Hypotension in Primary Care.

CONTINUING MEDICAL EDUCATION

LEARNING OBJECTIVES

* Classify patients by type of orthostatic hypotension

* Assess patients to arrive at a firm diagnosis

* Implement evidence-based treatment to alleviate symptoms, prevent complications, and improve quality of life

TARGET AUDIENCE

Family physicians and clinicians who wish to gain increased knowledge and greater competency regarding primary care management of orthostatic hypotension.

DISCLOSURES

As a continuing medical education provider accredited by the Accreditation Council for Continuing Medical Education (ACCME), Primary Care Education Consortium (PCEC) requires any individual in a position to influence educational content to disclose any financial interest or other personal relationship with any commercial interest. This includes any entity producing, marketing, re-selling or distributing health care goods or services consumed by, or used on, patients. Mechanisms are in place to identify and resolve any potential conflict of interest prior to the start of the activity. In addition, any discussion of off-label, experimental, or investigational use of drugs or devices will be disclosed by the faculty.

Dr. Jones discloses that she has no real or apparent conflicts of interest to report.

Dr. Kuritzky discloses that he is on the advisory board and speaker's bureau for Lundbeck LLC.

Gregory Scott, PharmD, RPh and Angela Cimmino, PharmD, editorial support, disclose they have no real or apparent conflicts of interest to report.

Michael Hanak, MD, CME Reviewer, discloses that he has no real or apparent conflicts of interest to report.

SPONSORSHIP

This activity is sponsored by Primary Care Education Consortium.

ACCREDITATION

The Primary Care Education Consortium is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

CREDIT DESIGNATION

AMA PRA Category 1--Primary Care Education Consortium designates this activity for a maximum of 1.0 AMA PRA Category 1 credit[TM]. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Release Date: 1 August 2018

Expiration Date: 31 July 2019

METHOD OF PARTICIPATION

PHYSICIANS

To receive CME credit, please read the journal article and on completion, go to www.pceconsortium.org/orthostatic to complete the online post-test and receive your certificate of completion.

PHYSICIAN ASSISTANTS

AAPA accepts certificates of participation of educational activities certified for AMA PRA Category 1 Credit[TM] from organizations accredited by ACCME or a recognized state medical society.

SUPPORTER

This article is supported by an educational grant from Lundbeck LLC.

INTRODUCTION

Orthostatic hypotension (OH) is associated with significant morbidity and potential loss of autonomy. In addition to increased risk of falls, OH is associated with an increased risk of heart failure, atrial fibrillation, kidney failure, hospitalization, stroke, cognitive impairment, and death. (1-6) The prevalence of chronic OH is underestimated and OH often is overlooked in common disorders, such as Parkinson's disease (PD) and diabetes mellitus. (7) Fortunately, there are effective nonpharmacologic and pharmacologic interventions available to improve quality of life and reduce the risk for devastating consequences, such as a fall or hip fracture. However, many clinicians neglect to screen for OH, missing the opportunity to treat.

DEFINITION AND EPIDEMIOLOGY

Maintenance of blood pressure (BP) upon standing requires a complex interaction between baroreceptors, the sympathetic nervous system, and the cardiovascular system. Defective compensatory responses can result from cardiac dysfunction, reduced intravascular volume, excessive vasodilation, baroreceptor dysfunction, autonomic nervous system impairment, or as a result of medications. (8,9)

OH generally has been defined as a sustained reduction of systolic BP (SBP) of 20 mm Hg or diastolic BP (DBP) of 10 mm Hg within 3 minutes of standing from a supine or seated position, or a tilt table head-up tilt of [greater than or equal to]60 degrees. (10) The authors do not suggest that tilt table testing be performed routinely; rather, OH should be a straightforward clinical diagnosis. Tilt testing could produce significant false positive results because the support of lower extremity musculature critical for maintaining normotension in the erect posture is eliminated during tilt table testing.

OH sometimes is comorbid with postural orthostatic tachycardia syndrome (POTS). POTS, which also causes lightheadedness or fainting as the primary symptom, is a condition in which an excessively reduced volume of blood returns to the heart when moving from the supine to the standing position. POTS is accompanied by a rapid increase in heart rate of [greater than or equal to]30 beats per minute (bpm). Most people who experience POTS are women between the ages of 15 and 50 years. (11)

Neurogenic OH (NOH), a commonly overlooked subtype of OH, is associated with nervous system impairment, and is predominantly seen in neurodegenerative disorders such as PD, multiple system atrophy (MSA), and pure autonomic failure (PAF). (10) NOH also might accompany peripheral and autonomic neuropathies associated with diabetes, amyloidosis, and immune-mediated neuropathies. (12) In primary or secondary diseases of the autonomic nervous system, NOH often is accompanied by supine hypertension. The prevalence of NOH is approximately 50% among patients with PD, and approximately 33% among those with diabetes, amyloidosis, or spinal cord injury. (1,13,14) Fortunately, only a portion of these patients are symptomatic at the time of OH diagnosis.

Patients at increased risk for OH should be screened even in the absence of symptoms; this includes those with PD, MSA, PAF, dementia with Lewy bodies, and peripheral neuropathies associated with autonomic dysfunction (eg, diabetes, amyloidosis, HIV). Patients with an unexplained fall or syncopal episode, elderly patients (age >70 years), and those on multiple medications that affect intravascular volume, vascular tone, sympathetic activity, or cardiac function also warrant screening. (15)

DIAGNOSIS

Typical OH symptoms, which occur when standing, less frequently when sitting, and abate when lying down, include dizziness, lightheadedness, blurred vision, weakness, fatigue, nausea, palpitations, and headache. Less common symptoms include syncope, dyspnea, chest pain, and neck and shoulder "coat hanger" pain. (16,17) Heat exposure, large or carbohydratedense meals, alcohol, dehydration, and medications with potential for vasodilation, volume depletion, bradycardia, or sympatholytic medications (eg, antihypertensives, tricyclic antidepressants, diuretics, dopaminergic anti-parkinsonian agents, and phosphodiesterase inhibitors) could exacerbate OH symptoms. (10,13,16) Nocturnal diuresis results in peak symptoms in the morning. (12,17) Among patients with autonomic dysfunction, supine hypertension commonly co-exists with NOH, and might exaggerate this overnight diuresis. (16)

The diagnosis of OH requires measuring BP in both the supine and upright positions. (10) To establish a baseline, BP and heart rate are measured after 5 minutes of rest in the supine or seated position. Ideally standing BP and heart rate are measured at 30 seconds, 60 seconds, 2 minutes, and 3 minutes; however, for practicality, some experts advocate using the 3-minute reading as the primary discriminator. (13) In situations where a supine to standing diagnostic assessment cannot be performed easily, a sit-to-stand procedure could be used. (18) Patients sit for at least 5 minutes and then stand for 3 minutes, with BP measured just before standing and at 1 and 3 minutes upon standing. (15) One investigation showed a decrease in SBP >15 mm Hg or DBP >7 mm Hg to yield the highest sensitivity and specificity for the diagnosis of OH. (18) Note that these criteria differ slightly from the criteria included in the definition of OH.

An increase in heart rate >15 bpm within 3 minutes of standing is consistent with non-neurogenic OH (eg, volume depletion). (15) An increase in heart rate <15 bpm on standing is suggestive of NOH caused by reduced sympathetic response. (15,17) Medications that impede an appropriate heart rate response and cardiac arrhythmias must be taken into account.

If standard orthostatic BP testing (including extended at-home BP monitoring or 24-hour ambulatory monitoring) does not reveal OH in an at-risk individual with unexplained postural symptoms, referral to a movement disorder specialist is necessary. (15) Presence of a potential cardiac etiology warrants referral to a cardiologist. (19)

History and physical examination are key to differentiating between NOH and non-neurogenic OH. Laboratory, electrocardiogram, and imaging assessments further aid in ruling out non-neurogenic causes such as dehydration, acute blood loss, cardiovascular disorders (eg, constrictive pericarditis, cardiomyopathy, aortic stenosis), endocrine disorders (eg, adrenal insufficiency, diabetes), and excessive vasodilatation (eg, systemic mastocytosis, carcinoid syndrome) (figure). (1,8,12,15) Patients should be queried about exacerbating factors that suggest an autonomic cause, eg, prolonged standing, cardiovascular exercise, heat exposure, alcohol, morning time, or large meals. (16) Laboratory evaluations could include basic metabolic panel, complete blood count, morning Cortisol level, vitamin B12, folic acid (peripheral neuropathy), and fasting plasma glucose or glycated hemoglobin. (15,20)

TREATMENT

There is insufficient evidence to support intervention for asymptomatic OH. The goal of treatment in symptomatic OH is not to normalize standing BP, but rather to alleviate symptoms, prevent falls, and improve standing time to allow for activities of daily living. Additionally, in patients with NOH, the goal is to minimize comorbid supine hypertension. (21) Management of OH addresses modifiable contributing factors (eg, medications, dehydration, anemia), and employs nonpharmacologic strategies, and, if necessary, pharmacologic treatment (figure). (1,8,12,15) Because orthostatic stress varies with circumstances during the day, a patient-oriented approach that emphasizes education and nonpharmacologic strategies to minimize orthostatic stress is vital. (9)

Nonpharmacologic strategies

Patients should be counseled to avoid situations that could exacerbate symptoms associated with OH such as prolonged or motionless standing, alcohol, large or carbohydrate-dense meals, physical activity sufficient to cause muscle vasodilation, heat exposure (eg, hot weather, hot bath), sudden postural changes, and Valsalva maneuvers. (9,17)

Evidence-based nonpharmacologic strategies can be employed to expand blood volume (increased fluid and salt intake), decrease nocturnal diuresis (raise the head of the bed), decrease venous pooling (abdominal binder, physical counter maneuvers [see online video demonstration at: https://www.youtube.com/watch?v=lLqOAN9AJoA&t= 352s]), or induce a pressor response (water bolus intake). (9) These strategies, and the evidence supporting them, are further detailed in the table. (1,9,12,16,17,21-27)

Pharmacologic strategies

Pharmacologic intervention is indicated when nonpharmacologic strategies and lifestyle modification do not sufficiently resolve OH symptoms. Pharmacologic strategies aim to expand intravascular volume (fludrocortisone) or increase peripheral vascular resistance with the pressor agents midodrine or droxidopa. (17) Because of the prevalence of supine hypertension among patients with OH (up to 50%), slow titration and frequent monitoring is advised. (12,16) Home BP monitoring is recommended for several days after starting or changing therapy. (15)

Fludrocortisone

Fludrocortisone, a synthetic mineralocorticoid, is an aldosterone receptor agonist. It increases plasma volume by increasing renal sodium and water reabsorption and improves vascular alpha-adrenoreceptor sensitivity to circulating catecholamines. Fludrocortisone monotherapy could be considered for patients who do not adequately raise plasma volume with fluid and salt supplementation. Fludrocortisone may also be added to midodrine in patients with persistent OH symptoms. (9,12)

The initial dose of fludrocortisone is 0.1 mg/d, which can be titrated to 0.2 mg/d. Daily dosages >0.2 mg rarely are more effective and amplify side effects. (17) A weight gain of 3 to 5 pounds and mild dependent edema is indicative of adequate plasma volume expansion. (9,19) The onset of action typically is 3 to 7 days, but may require up to 2 weeks. (15,17) Because hypokalemia can develop in nearly 50% of patients and hypomagnesemia in 5%, electrolyte monitoring is required, and patients should be counseled to increase dietary potassium. Other common adverse events include supine hypertension, nausea, peripheral edema, and headache. (1,16)

Midodrine

Midodrine is a peripherally selective alpha-1-adrenoreceptor agonist that constricts arteriolar and venous vasculature resulting in supine, sitting, and standing SBP and DBP increases. (17) Double-blind multicenter placebo-controlled trials have shown midodrine to increase standing BP and improve OH symptoms. (28,29) In dose-response trials, midodrine, 10 mg, compared with placebo produced an average 1-minute standing SBP increase at 1 hour of 15 mm Hg. (30) This drug is approved for treating symptomatic OH. (30)

Midodrine is dosed in 4-hour intervals 3 times a day; eg, shortly before or upon arising in the morning, midday, and late afternoon before 6 pm. Dosages are titrated to clinical response or maximum daily dosage of 30 mg. The evening dose should be taken 3-4 hours before bedtime because of risk of supine hypertension in up to 25% of patients. (19) The medication should be discontinued in patients who do not have significant symptomatic improvement. (13,16) Midodrine can be used as monotherapy or in combination with fludrocortisone or, in low dosages, with pyridostigmine. (19,31) Adverse events include urinary urgency or retention (6%), piloerection (13%), pruritus/tingling (mostly of scalp; 9% to 10%), and chills (5%). (19)

Droxidopa

Droxidopa is a prodrug converted to norepinephrine in the central nervous system and peripheral tissues, including sympathetic peripheral nerve endings. Droxidopa is approved for treatment of symptomatic NOH caused by primary autonomic failure (PD, MSA, PAF), dopamine betahydroxylase deficiency, and nondiabetic autonomic neuropathy. (32) Droxidopa is only available through specialty pharmacies and requires that the prescriber submits a treatment form indicating primary diagnosis, symptomatic condition, treatment history, and patient clinical notes. (33)

An integrated efficacy analysis of 3 clinical trials comparing droxidopa with placebo in patients with a primary neurodegenerative disease and symptomatic NOH (N=460) showed significant reduction in most NOH symptom scores: Orthostatic Hypotension Questionnaire composite score, dizziness/lightheadedness, visual disturbances, weakness, and fatigue. (34) Droxidopa also significantly improved 3 of 4 patient-oriented measures and significantly increased upright SBP (11.5 [+ or -] 20.5 vs 4.8 [+ or -] 21 mm Hg; P<.001) and DBP (8 [+ or -] 15.55 vs 1.8 [+ or -] 17.3 mm Hg; P<.001). (34) Alower incidence of falls was observed in the droxidopa group. (34)

The starting dosage of droxidopa is 100 mg three times daily, titrated by 100 mg three times daily to a maximum dosage of 600 mg three times daily. The last daily dose should be at least 3 hours before bedtime and the head of bed should be elevated to minimize supine hypertension. (32) The rates of supine hypertension (SBP >180 mm Hg) in clinical trials were [less than or equal to]7.9% with droxidopa vs [less than or equal to]4.6% with placebo. (34) Adverse effects include hypertension, headache, dizziness, and nausea. (14)

Pyridostigmine

Pyridostigmine, an acetylcholinesterase inhibitor that potentiates neurotransmissionin autonomic ganglia, amplifies sympathetic activation in response to orthostatic stress. Pyridostigmine has been used off-label as monotherapy in patients with mild symptoms, and as an adjunct to low-dose midodrine (2.5 mgonce ortwice daily). (15,31) In a double-blind, 4-way crossover study in patients with NOH (n=58), pyridostigmine, 60 mg either alone or with 2.5 mg, or midodrine, 5 mg, produced smaller reductions in standing DBP vs placebo with no effect on supine SBP or DBP. (31) Because pyridostigmine is not associated with worsening supine hypertension, it could be considered when supine hypertension becomes problematic. (31) The starting dosage of pyridostigmine is 30 mg two or three times daily, and can be increased to 60 mg three times daily. (9) Adverse effects include diaphoresis, hypersalivation, diarrhea, muscle cramping, and urinary incontinence. (15,16)

SPECIAL CONSIDERATIONS

Supine and nocturnal hypertension

Although most patients with essential hypertension experience BP elevation throughout the day and night--albeit to a lesser degree at night by 10% to 20%--patients with supine HTN experience HTN only at night. Although the potential long-term effects of supine HTN should not be minimized, it should be recognized that the risks of supine HTN remain uncertain with no clinical trials documenting benefit from treating supine HTN. The short-term risks associated with NOH (ie, falls and hip fractures) could take precedence over the longer-term theoretical risks associated with supine HTN (ie, cerebrovascular and cardiovascular events). (35) Paradoxically, untreated supine HTN can worsen OH by causing pressure natriuresis and diuresis, resulting in volume depletion. (35) To minimize episodes of supine HTN, patients should avoid recumbency during the day, raise the head of the bed, and avoid fluids within 1 hour of bedtime. (13) If these measures are insufficient, a short-acting antihypertensive at bedtime could be considered (eg, angiotensin II receptor blocker, short-acting angiotensin-converting enzyme inhibitor, nifedipine, clonidine, or a nitrate patch [removed 1 hour before rising]). (13)

Postprandial hypotension

Among patients with autonomic dysfunction, 40% to 80% of patients also have postprandial hypotension. (36) This is commonly defined as a decline in SBP [greater than or equal to]20 mm Hg within 2 hours of consuming a meal or decline of SBP to <90 mm Hg when preprandial SBP is >100 mm Hg. (37) Large and carbohydrate-heavy meals induce splanchnic vasodilation and redistribution of blood flow to the digestive system. (16) Patients are advised to avoid carbohydrate-heavy meals, alcohol, and sudden standing or physical activity after a meal. (12) Treatment with the alpha-glucosidase inhibitor acarbose could be considered because it delays intestinal glucose absorption by inhibiting complex carbohydrate breakdown, thereby delaying release of vasodilatory gut hormones. (35,38)

SUMMARY

A fall of SBP [greater than or equal to]20 mm Hg or in DBP [greater than or equal to]10 mm Hg within 3 minutes of standing is diagnostic of OH. History and physical examination are key to differentiating between neurogenic and non-neurogenic OH. To achieve the primary goals of reducing symptoms and preventing falls, treatment of OH is directed at increasing blood volume, decreasing venous pooling, and increasing vasoconstriction. Reversible causes of OH (dehydration, hypotensive medications) should be investigated. Patient education and nonpharmacologic strategies alone can be effective in mild cases of OH. If symptoms persist, consider low-dosage fludrocortisone. Other pharmacologic options include droxidopa, pyridostigmine, or an [alpha]-adrenoreceptor agonist such as midodrine. For patients with NOH, worsening of supine HTN should be evaluated and proactively managed. Because OH can have devastating consequences for some patients, identifying persons at increased risk is imperative. Avoiding falls by successfully managing OH has the potential to reduce morbidity and mortality.

DISCLOSURES

Dr. Jones discloses that she has no real or apparent conflicts of interest to report.

Dr. Kuritzky discloses that he is on the advisory board and speakers' bureau for Lundbeck LLC.

ACKNOWLEDGEMENT

Editorial support was provided by Gregory Scott, PharmD, RPh, and Angela Cimmino, PharmD. The authors were responsible for all content and editorial decisions.

SUPPORT

This article is sponsored by Primary Care Education Consortium and supported by funding from Lundbeck LLC.

REFERENCES

(1.) Fedorowski A, Melander O. Syndromes of orthostatic intolerance: a hidden danger. J Intern Med. 2013;273(4):322-335.

(2.) Veronese N, De Rui M, Bolzetta F, et al. Orthostatic changes in blood pressure and mortality in the elderly: The Pro.V.A Study. Am J Hypertension. 2015;28(10):1248-1256.

(3.) Ricci F, Fedorowski A, Radico F, et al. Cardiovascular morbidity and mortality related to orthostatic hypotension: a meta-analysis of prospective observational studies. Eur Heart J. 2015;36(25):1609-1617.

(4.) Rose KM, Eigenbrodt ML, Biga RL, et al. Orthostatic hypotension predicts mortality in middle-aged adults: the Atherosclerosis Risk In Communities (ARIC) Study. Circulation. 2006;114(7):630-636.

(5.) Masaki KH, Schatz I), Burchfiel CM, et al. Orthostatic hypotension predicts mortality in elderly men: the Honolulu Heart Program. Circulation. 1998:98(21): 2290-2295.

(6.) Verwoert GC, Mattace-Raso FU, Hofman A, et al. Orthostatic hypotension and risk of cardiovascular disease in elderly people: the Rotterdam study. J Am Geriatr Soc. 2008;56(10):1816-1820.

(7.) Robertson D, Robertson RM. Causes of chronic orthostatic hypotension. Arch Intern Med. 1994;154(14):1620-1624.

(8.) Kuritzky L, Espay AJ, Gelblum J, Payne R, Dietrich E. Diagnosing and treating neurogenic orthostatic hypotension in primary care. Postgrad Med 2015;127(7):702-715.

(9.) Figueroa JJ, Basford JR, Low PA. Preventing and treating orthostatic hypotension: as easy as A, B, C. Cleve Clin J Med 20I0;77(5):298-306.

(10.) Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res. 2011;21(2):69-72.

(11.) American Academy of Neurology. Postural tachycardia syndrome. 2018. http://patients. aan.com/disorders/index.cfm?event=view&disorderjd=1044. Accessed March 19, 2018.

(12.) Freeman R. Neurogenic orthostatic hypotension. N Engl J Med. 2008;358:615-624.

(13.) Chisholm P, Anpalahan M. Orthostatic hypotension: pathophysiology, assessment, treatment and the paradox of supine hypertension. Intern Med J. 2017;47(4):370-379.

(14.) Eschlbock S, Wenning G, Fanciulli A. Evidence-based treatment of neurogenic orthostatic hypotension and related symptoms. J Neural Transm. 2017;124(12):1567-1605.

(15.) Gibbons CH, Schmidt P, Biaggioni I, et al. The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension. J Neurol. 2017;264(8):1567-1582.

(16.) Berger MJ, Kimpinski K. A practical guide to the treatment of neurogenic orthostatic hypotension. Can J Neurol Sci. 2014;41(2):156-163.

(17.) Palma JA, Kaufmann H. Epidemiology, diagnosis, and management of neurogenic orthostatic hypotension. Mov Disord Clin Pract. 2017;4(3):298-308.

(18.) Shaw BH, Garland EM, Black BK, et al. Optimal diagnostic thresholds for diagnosis of orthostatic hypotension with a 'sit-to-stand test' J Hypertens. 2017;35(5):1019-1025.

(19.) Lahrmann H, Cortelli P, Hilz M, Mathias CJ, Struhal W, Tassinari M. EFNS guidelines on the diagnosis and management of orthostatic hypotension. Eur J Neurol 2006; 13(9):930-936.

(20.) Lanier JB, Mote MB, Clay EC. Evaluation and management of orthostatic hypotension. Am Fam Physician. 2011;84(5):527-536.

(21.) Low PA, Tomalia VA. Orthostatic hypotension: mechanisms, causes, management. J Clin Neurol. 2015;ll(3):220-226.

(22.) Denq JC, Opfer-Gehrking TL, Giuliani M, Felten J, Convertino VA, Low PA. Efficacy of compression of different capacitance beds in the amelioration of orthostatic hypotension. Clin Auton Res 1997;7(6):321-326.

(23.) Jordan J, Shannon JR, Black BK, et al. The pressor response to water drinking in humans: a sympathetic reflex? Circutoion. 2000;101(5):504-509.

(24.) Jordan J, Shannon JR, Grogan E, Biaggioni I, Robertson D. A potent pressor response elicited by drinking water. Lancet. 1999;353(9154):723.

(25.) May M, Jordan J. The osmopressor response to water drinking. Am J Physiol Regul Integr Comp Physiol. 2011;300(1):R40-46.

(26.) Mtinangi BL, Hainsworth R. Early effects of oral salt on plasma volume, orthostatic tolerance, and baroreceptor sensitivity in patients with syncope. Clin Auton Res. 1998;8(4):231-235.

(27.) Smeenk HE, Koster MJ, Faaij RA, de Geer DB, Hamaker ME. Compression therapy in patients with orthostatic hypotension: a systematic review. Netherlands J Med 2014;72(2):80-85.

(28.) Low PA, Gilden JL, Freeman R, Sheng KN, McElligott MA. Efficacy of midodrine vs placebo in neurogenic orthostatic hypotension. A randomized, double-blind multicenter study. Midodrine Study Group. JAMA. 1997;277(13):1046-1051.

(29.) Wright RA, Kaufmann HC, Perera R, et al. A double-blind, dose-response study of midodrine in neurogenic orthostatic hypotension. Neurology. 1998;51(1):120-124.

(30.) Midodrine [package insert], Morgantown, WV: Mylan Pharmaceuticals Inc.; 2017.

(31.) Singer W, Sandroni P, Opfer-Gehrking TL, et al. Pyridostigmine treatment trial in neurogenic orthostatic hypotension. Arch Neurol. 2006;63(4):513-518.

(32.) Northera [package insert]. Deerfield, IL: Lundbeck Pharmaceuticals LLC; 2017.

(33.) Northera. Northera Treatment and Prescription Forms 2017; https://www.northeraemollment.com/. Accessed December 2,2017.

(34.) Biaggioni I, Arthur Hewitt L, Rowse GJ, Kaufmann H. Integrated analysis of droxidopa trials for neurogenic orthostatic hypotension. BMC Neurol. 2017;17(1):90.

(35.) Espay AJ, LeWitt PA, Hauser RA, Merola A, Masellis M, Lang AE. Neurogenic orthostatic hypotension and supine hypertension in Parkinson's disease and related synucleinopathies: prioritisation of treatment targets. Lancet Neurol. 2016;15(9):954-966.

(36.) Jones PK, Shaw BH, Raj SR. Orthostatic hypotension: managing a difficult problem. Expert Rev Cardiovasc Ther. 2015;13(11):1263-1276.

(37.) Jansen RW. Postprandial hypotension: simple treatment but difficulties with the diagnosis. J Gerontol A Biol Sci Med Sci 2005;60(10):1268-1270.

(38.) Shibao C, Gamboa A, Diedrich A, et al. Acarbose, an alpha-glucosidase inhibitor, attenuates postprandial hypotension in autonomic failure. Hypertension. 2007;50(1):54-61.

Jennifer Jones, MD, UCF College of Medicine-HCA Consortium Family Medicine Residency, Gainesville, Florida

Louis Kuritzky, MD, Clinical Assistant Professor Emeritus, Department of Community Health and Family Medicine, College of Medicine, University of Florida, Gainesville, Florida

Caption: FIGURE Diagnostic and treatment algorithm for orthostatic hypotension (1,8,12,15)
TABLE Nonpharmacologic interventions for treating orthostatic
hypotension (19,12,16,17,21-27)

Intervention          Specific Instructions    Comments
Dietary counseling    2 to 2.5 liters of       Clear urine provides
and recommendations   fluid/d                  patient with a visual
                      10 g-d sodium intake     target for maintaining
                      (1-2 teaspoons of        adequate hydration
                      added salt to a          Benefits of salt
                      healthy diet; 0.5-1 g    loading can be seen as
                      salt tablets)            early as 3 days after
                      Avoid diuretics,         initiation
                      including coffee         24-hour urinary sodium
                      Avoid high glycemic      excretion [greater
                      index meals/beverages    than or equal to]170
                                               mmoL and 24-hour urine
                                               output of 1.5 liters
                                               are indicative of
                                               adequate salt loading
                                               and plasma volume
Water bolus           Drink 500 mL of water    Raises SBP [greater
                      over 3 to 4 minutes      than or equal to]20 mm
                                               Hg within 5-15
                                               minutes; peaks at 20-
                                               30 minutes; lasts for
                                               1-2 hours
                                               Anticipatory
                                               management (eg,
                                               prolonged standing,
                                               hot weather,
                                               preprandial, upon
                                               awakening)
Physical counter-     Perform physical         Counter-maneuvers can
maneuvers and         counter-maneuvers, eg,   be done to attenuate
exercise              crossing legs, trunk     OH symptoms at onset
                      bending, squatting,      Rise gradually from
                      knee flexing, toe        lying to sitting to
                      raises, tensing          standing, especially
                      muscles (contract a      in the morning when
                      group of muscles         orthostatic tolerance
                      bilaterally for 30       is lower or after
                      seconds, relax, and      meals or straining
                      then repeat)             with defecation
                      Gradual staged           Exercise in a
                      movements with           recumbent or seated
                      postural changes         position or in a pool
                      Elevate head of the      to attenuate exercise-
                      bed 6-9 inches           induced hypotension,
                      Avoid daytime            which accompanies
                      recumbency               deconditioned states
                      Avoid Valsalva
                      maneuvers
                      Isotonic exercises
Compression           Abdominal binder and-    Splanchnic-mesenteric
garments              or custom-fitted thigh   venous bed compression
                      or waist high            reduces venous pooling
                      compression stockings    and drop in SBP after
                                               postural changes
                                               Should be tight enough
                                               to exert gentle
                                               pressure
                                               Place before rising
                                               from bed in the
                                               morning, and take off
                                               when lying supine
                                               May use as needed
                                               during times of
                                               orthostatic stress
                                               More effective than
                                               lower extremity
                                               compression
                                               Migh be difficult for
                                               patients to put on,
                                               uncomportable, and
                                               cosmetically
                                               unappealing

Abbreviations: OH, orthostatic hypotension; SBP, systolic blood
pressure.
COPYRIGHT 2018 Quadrant Healthcom, Inc.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2018 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Jones, Jennifer; Kuritzky, Louis
Publication:Journal of Family Practice
Article Type:Clinical report
Geographic Code:1USA
Date:Aug 1, 2018
Words:4340
Previous Article:Long-term Treatment of Gout: New Opportunities for Improved Outcomes.
Next Article:Practical Evaluation and Management of Irritable Bowel Syndrome with Diarrhea: A Case Study Approach.
Topics:

Terms of use | Privacy policy | Copyright © 2021 Farlex, Inc. | Feedback | For webmasters |