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1st Year Fellow – Geriatric Medicine Baylor College of Medicine

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1 1st Year Fellow – Geriatric Medicine Baylor College of Medicine
GERIATRIC MEDICINE GRAND ROUNDS January 5th, TOPIC ORTHOSTATIC HYPOTENSION IN ELDERLY PRESENTER Aman Haider, MD 1st Year Fellow – Geriatric Medicine Baylor College of Medicine

2 Sections Introduction , Definitions & Background of Orthostatic Hypotension (OH) Epidemiology of OH Pathogenesis of OH Etiology of OH Clinical Presentation of OH Evaluation of OH Management of OH

3 DEFINITION & BACKGROUND ORTHOSTATIC HYPOTENSION
INTRODUCTION , DEFINITION & BACKGROUND OF ORTHOSTATIC HYPOTENSION

4 Introduction Orthostatic (postural) hypotension (OH) is a common disorder. Frequently under diagnosed. Frequent cause of syncope. Contributes to morbidity, disability and even mortality. It is a SYNDROME, and its prognosis depends on : Its Specific Cause Its Severity The Distribution of its Autonomic or Non-Autonomic involvement.

5 Definition ORTHOSTATIC HYPOTENSION is a reduction of …
Systolic blood pressure of at least 20 mm Hg OR Diastolic blood pressure of at least 10 mm Hg Within 3 minutes of standing. An acceptable alternative to STANDING : Demonstration of a similar drop in blood pressure within 3 minutes Using a tilt table in the head-up position At an angle of at least 60 degrees Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Neurology 1996;46:1470 A Consensus Conference was held on November 16th, which was sponsored by the American Autonomic Society, and co-sponsored by the American Academy of Neurology with the specific aim of generating a consensus on three specific items: - the definition of orthostatic hypotension, - pure autonomic failure (idiopathic orthostatic hypotension, progressive autonomic failure), and - multiple system atrophy. 2) They defined the orthostatic hypotension as such : Orthostatic hypotension (OH) is a reduction of … - systolic blood pressure of at least 20 mm Hg OR - diastolic blood pressure of at least 10 mm Hg - within 3 minutes of standing.

6 Limitations of Definition
Does not take into account : The possibility that different blood pressure declines may have different clinical significance. Blood pressure changes that may occur after 3 minutes of standing. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Neurology 1996;46:1470

7 Confounding Variables
Should be considered before making the diagnosis : Food ingestion Recent recumbency Time of day State of hydration Ambient temperature Postural deconditioning Hypertension and anti-hypertensive medications Gender Age Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Neurology 1996;46:1470

8 EPIDEMIOLOGY OF ORTHOSTATIC HYPOTENSION

9 Prevalence Among Nursing Home Residents
One Study to “Determine Patterns Of Within-day Orthostatic Blood Pressure Changes” Cross Sectional study with 911 residents from 45 nursing homes . Aged 60 years or older, able to stand for at least 1 minute. Supine ,1-minute and 3-minute standing BP + HR were measured. Before and after breakfast and before and after lunch. No OH = 48.5% Only once = 18.3% 2-3 times = 19.9% 4 or more times = 13.3% Most prevalent before breakfast, especially 1 minute after standing (21.3%) Least prevalent after lunch, after 3 minutes of standing (4.9%) Ooi WL, Barrett S, Hossain M, Kelley-Gagnon M, Lipsitz LA. Patterns of orthostatic blood pressure change and their clinical correlates in a frail, elderly population. JAMA Apr 23-30; 277(16):

10 Prevalence In Community- Dwelling Elderly
A study to “Assess Prevalence of Orthostatic Hypotension and its Associations”. A multicenter, observational, longitudinal study . Enrolled 5,201 men and women aged >65 yrs. Prevalence 14.8% for those age 65 to 69 and 26% for those age >85 OH was associated significantly with : Difficulty walking (odds ratio, 1.23) Frequent falls (odds ratio, 1.52) H/o MI (odds ratio, 1.24) H/o TIA (odds ratio, 1.68) Isolated systolic hypertension (odds ratio, 1.35) Major EKG abnormalities (odds ratio, 1.21) Presence of carotid artery stenosis based on ultrasound (odds ratio, 1.67) Negatively associated with weight. Rutan GH, et al. Orthostatic hypotension in older patients. The cardiovascular health study. CHS collaborative research group. Hypertension. 19(6 Pt 1): , June 1992 The purpose of the present study was to assess the prevalence of orthostatic hypotension and its associations with demographic characteristics, cardiovascular risk factors and symptomatology, prevalent cardiovascular disease, and selected clinical measurements in the Cardiovascular Health Study a multicenter, observational, longitudinal study enrolling 5,201 men and women aged 65 years and older at initial examination. Blood pressure measurements were obtained with the subjects in a supine position and after they had been standing for 3 minutes. The prevalence of asymptomatic orthostatic hypotension, defined as 20 mm Hg or greater decrease in systolic or 10 mm Hg or greater decrease in diastolic blood pressure, was 16.2%. This prevalence increased to 18.2% when the definition also included those in whom the procedure was aborted due to dizziness upon standing. The prevalence was higher at successive ages. Orthostatic hypotension was associated significantly with difficulty walking (odds ratio, 1.23; 95% confidence interval, 1.02, 1.46), frequent falls (odds ratio, 1.52; confidence interval, 1.04, 2.22) histories of myocardial infarction (odds ratio, 1.24; confidence interval, 1.02,130) H/O transient ischemic attacks (odds ratio, 1.68; confidence interval, 1.12, 2.51) isolated systolic hypertension (odds ratio, 135; confidence interval, 1.09, 1.68), major electrocardiographic abnormalities (odds ratio, 1.21; confidence interval, 1.03, 1.42) presence of carotid artery stenosis based on ultrasonography (odds ratio, 1.67; confidence interval, 1.23, 2.26). Orthostatic hypotension was negatively associated with weight

11 PATHOGENESIS OF ORTHOSTATIC HYPOTENSION

12 Normal Postural Changes in BP
Normal BP response on moving from a supine to a standing position : Small reduction (<10 mm Hg) in SBP & increase in DBP (~ 2.5 mm Hg). Gravity Induced Drop  Approximately 500 to 1000 ml of blood is pooled in the lower extremities and in the splanchnic and pulmonary circulations. Response (Baroreflex) : Gravity Induced Drop Decreased venous return to the heart Transient reduction in CO and BP Stimulation of the baroreceptors in carotid arteries and aorta Reflexively increased sympathetic tone  Increased PVR (Vasoconstriction) Inhibits parasympathetic activity  Increased HR Restoration of CO and BP by an increase in HR and PVR. baroreflex; it is mediated by afferent and efferent autonomic peripheral nerves and is integrated in autonomic centers in the brainstem. Orthostatic hypotension is the result of baroreflex failure (autonomic failure), endorgan dysfunction, or volume depletion. Injury to any limb of the baroreflex causes neurogenic orthostatic hypotension, although with afferent lesions alone, the hypotension tends to be modest and accompanied by wide fluctuations in blood pressure, including severe hypertension. Drugs can produce orthostatic hypotension by interfering with the autonomic pathways or their target end-organs or by affecting intravascular volume. Brain hypoperfusion, resulting from orthostatic hypotension from any cause, can lead to symptoms of orthostatic intolerance (eg, lightheadedness) and falls, and if the hypotension is severe, to syncope.

13 Postural Changes in Elderly
“Age-Related Changes” that can effect normal BP Regulation :

14 ETIOLOGY OF ORTHOSTATIC HYPOTENSION

15 Etiology Causes of orthostatic hypotension can be broadly divided into acute and chronic Acute orthostatic hypotension most commonly develops over a relatively short period of time and is more often symptomatic at the outset. - Adrenal insufficiency, myocardial ischemia, medication administration, sepsis, or dehydration Chronic orthostatic hypotension develops gradually over a prolonged period of time and the patient is usually asymptomatic during the initial period - PHYSIOLOGIC CAUSES are those attributable to the age-associated changes in blood pressure regulation described above, as well as the age related increase in systolic blood pressure, which further impairs adaptive responses to hypotensive stresses. These physiologic changes predispose elderly people to symptomatic hypotension in the face of common everyday stresses, such as posture change, meals, new medications, fluid restriction, or any acute illness. - PATHOLOGIC CAUSES of chronic orthostatic hypotension are secondary to central or peripheral nervous system diseases that result in autonomic insufficiency Orthostatic hypotension may result from neurogenic and nonneurogenic causes. Neurogenic orthostatic hypotension can be due to neuropathy (eg, diabetic or autoimmune neuropathies) or to central lesions (eg, Parkinson disease or multiple system atrophy). Its presence, severity, and temporal course can be important clues in diagnosing Parkinson disease and differentiating it from other parkinsonian syndromes with a more ominous prognosis, such as multiple system atrophy and Lewy body dementia. Nonneurogenic causes include cardiac impairment (eg, from myocardial infarction or aortic stenosis), reduced intravascular volume (eg, from dehydration, adrenal insufficiency), and vasodilation (eg, from fever, systemic mastocytosis). Common drugs that cause orthostatic hypotension are diuretics, alpha-adrenoceptor blockers for prostatic hypertrophy, antihypertensive drugs, and calcium channel blockers. Insulin, levodopa, and tricyclic antidepressants can also cause vasodilation and orthostatic hypotension in predisposed patients. Poon and Braun,6 in a retrospective study in elderly veterans, identified hydrochlorothiazide, lisinopril (Prinivil, Zestril), trazodone (Desyrel), furosemide (Lasix), and terazosin (Hytrin) as the most common culprits. Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. Am J Med 2007 Oct; 120 (10):

16 Drug that may Worsen OH A retrospective study in elderly veterans, identified hydrochlorothiazide, lisinopril (prinivil, zestril), trazodone (desyrel), furosemide (lasix), and terazosin (Hytrin) as the most common culprits. Figueroa JJ, Basford JR, Low PA, Preventing and treating orthostatic hypotension: As easy as A, B, C. Cleve Clin J Med, 77:2010,

17 CLINICAL FEATURES OF ORTHOSTATIC HYPOTENSION

18 Symptoms Symptoms that develop … On assuming erect posture, OR
Following head-up tilt, and usually Resolve on resuming the recumbent position. Symptoms include : Lightheadedness, dizziness, blurred vision, weakness, fatigue, cognitive impairment, nausea, palpitations, tremulousness, headache, and neck ache (Coat Hanger Ache) Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Neurology 1996;46:1470. In Elderly, disturbed speech, visual changes, falls, confusion, and impaired cognition are more common. Rutan GH, Hermanson B, Bild DE, et al. Orthostatic hypotension in older adults. The Cardiovascular Health Study. Hypertension. 1992; 19: Symptoms are related to cerebral hypoperfusion, with resulting lack of cerebral oxygenation causing lightheadedness, dizziness, weakness, difficulty thinking, headache, syn-cope, or feeling faint) and a compensatory autonomic overreaction (causing palpitations, tremulousness, nausea, coldness of extremities, chest pain, and syncope).

19 OH – A Predictor of Mortality
Orthostatic Hypotension Predicts Mortality in Elderly Men The Honolulu Heart Program A cohort of 3522 Japanese American men 71 to 93 years old. Total of 473 deaths in the cohort over 4 years. 52 of those who died had orthostatic hypotension 4 year all cause mortality = Relative Risk 1.64 ( 95% CI 1.19 to 2.26 ** ) ** With the use of Cox proportional hazards models, after adjustment for age, smoking, diabetes mellitus, body mass index, physical activity, seated systolic blood pressure, antihypertensive medications, hematocrit, alcohol intake, and prevalent stroke, coronary heart disease and cancer Masaki KH, Schatz IJ and Burchfiel CM. Orthostatic hypotension predicts mortality in elderly men: the Honolulu Heart Program. Circulation. 1998; 98:

20 Prognosis Of OH In patients who have extrapyramidal and cerebellar disorders (eg, PD , MSA) The earlier and the more severe the involvement of the autonomic nervous system, the poorer the prognosis - Sandroni P, Ahlskog JE, Fealey RD, Low PA. Autonomic involvement in extrapyramidal and cerebellar disorders. Clin Auton Res 1991; 1:147–155. - Saito Y, Matsuoka Y, Takahashi A, Ohno Y. Survival of patients with multiple system atrophy. Intern Med 1994; 33:321–325. In hypertensive patients with diabetes mellitus, the risk of death is higher if they have orthostatic hypotension. Luukinen H, Koski K, Laippala P, Kivelä SL. Prognosis of diastolic and systolic orthostatic hypotension in older persons. Arch Intern Med 1999; 159:273–280. Diastolic OH is associated with a higher risk of vascular death in older persons. Hoeldtke RD, Streeten DH. Treatment of orthostatic hypotension with erythropoietin. N Engl J Med 1993; 329:611–615.

21 EVALUATION OF ORTHOSTATIC HYPOTENSION

22 Evaluation In ER Setting
Syncope may be the initial presentation. A study to evaluate cause of syncope in 611 patients presenting at the ER. 24 % had orthostatic hypotension. Sarasin FP, Louis-Simonet M, Carballo D, et al. Prospective evaluation of patients with syncope: a population-based study. Am J Med. Aug ;111(3):177-84

23 Evaluation In Inpatient Care Setting
The annual nationwide inpatient sample (NIS), sponsored by the AHRQ During 2004, 80,095 orthostatic hypotension- related hospitalizations. OH listed as the primary diagnosis in 28,073 (35%) hospitalizations. Most frequent secondary diagnoses were : Atrial fibrillation (10.7%) Hypertension (8.9%) Syncope (8.2%) Chronic obstructive pulmonary disease (7.7%) Congestive heart failure (6.7%) Urinary tract infection (4.6%) Shibao C, Grijalva CG, Raj SR, Biaggioni I, Griffin MR. Orthostatic hypotension-related hospitalizations in the United States. Am J Med Nov;120(11):975-80

24 Evaluation In Outpatient Care Setting
More likely to have Chronic Etiologies Referred from the ER or hospital upon discharge for further testing. Usually have vague/ undifferentiated symptom description. Discontinuing vs changing medications MRI can be used to assess for possible etiologies of neurogenic orthostatic hypotension. Further testing as indicated.

25 Evaluation Evaluation Of Suspected OH
Begins by identifying reversible causes Underlying associated medical conditions. In addition to assessing for symptoms of orthostasis Elicit symptoms of autonomic dysfunction involving the GI and GU tract. Detailed assessment of the motor nervous system should be performed to evaluate for signs of parkinson’s disease, as well as cerebellar ataxia.

26 Evaluation of Orthostatic Hypotension
Initial evaluation should include measuring blood pressure and heart rate after the patient has been quietly supine for at least 5 minutes and again after 1 minute and 3 minutes of standing. Early morning measurements, especially after a high carbohydrate meal, are useful to identify postprandial hypotension. Although postprandial hypotension may occur concomitantly with orthostatic hypotension, it is a distinct entity that often occurs while sitting after a meal, and may actually resolve upon standing up and walking. Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. Am J Med 2007 Oct; 120 (10):

27 HistorY HISTORICAL FEATURES POSSIBLE ETIOLOGY Abnormal Uterine Bleeding, Fatigue, Rectal Bleeding Anemia Amaurosis Fugax, Aphasia, Dysarthria, Unilateral Sensory & Motor Symptoms Stroke Bradykinesia, Pill-rolling Tremor, Shuffling Gait Parkinson Disease Burns Intravascular Volume Depletion Chest Pain, Palpitations, Shortness Of Breath CHF, MI, Myocarditis, Pericarditis Chills, Fever, Lethargy, Nausea, Vomiting Gastroenteritis, Sepsis Extremity Swelling CHF, Venous Insufficiency High-risk Sexual Behavior AIDS, Neurosyphilis Progressive Motor Weakness GBS , Multiple System Atrophy Relapsing Neurologic Symptoms In Various Anatomic Locations Multiple Sclerosis Symptoms After A Meal Postprandial Hypotension Once the diagnosis of orthostatic hypotension is established, a detailed history should be obtained, focusing on medications (both prescription and nonprescription), volume losses (vomiting, diarrhea, fluid restriction), coexisting medical disorders, and autonomic dysfunction. Evaluation and Management of Orthostatic Hypotension ; American Family Physician Volume 84, Number 5 ; September 1, 2011

28 PHYSICAL EXAM Obtain Orthostatic Vital Signs.
Supine Blood Pressure and pulse after 3 minutes Standing Blood Pressure and pulse after 3 minutes As many as 2/3rd of patients may go undetected if BP is not measured while supine. Carlson JE. Assessment of orthostatic blood pressure:measurement technique and clinical applications. South Med J 1999; 92: 167–173. One retrospective review of 730 patients found that vital signs had poor test characteristics when compared with tilt-table testing for the diagnosis of OH. PPV = 61.7 % NPV= 50.2 % Cooke J, Carew S, O’Connor M, Costelloe A, Sheehy T, Lyons D. Sitting and standing blood pressure measurements are not accurate for the diagnosis of orthostatic hypotension. QJM. 2009;102(5):

29 Physical Exam Aphasia, Dysarthria, Facial Droop, Hemiparesis Stroke
EXAMINATION FINDINGS POSSIBLE DIAGNOSIS Aphasia, Dysarthria, Facial Droop, Hemiparesis Stroke Cogwheel Rigidity, Festinating Gait, Lack Of Truncal Rotation While Turning, Masked Facies Parkinson Disease Confusion, Dry Mucous Membranes, Dry Tongue, Longitudinal Tongue Furrows, Speech Difficulty, Sunken Eyes, Upper Body Weakness Dehydration (In Older Patients) Decreased Libido, Impotence In Men; Urinary Retention And Incontinence In Women Pure Autonomic Failure. Dependent Lower Extremity Edema, Stasis Dermatitis Right-sided Congestive Heart Failure, Venous Insufficiency Gummas, Unequal Pupils (Argyll Robertson Pupil) Loss Of Position And Vibration Senses Tabes Dorsalis Early Satiety, Postprandial Fullness, Constipation, Incontinence, Exercise Intolerance Diabetic Neuropathy Smooth Beefy Red Tongue, Lemon Pallor, Recent Loss Of Mental Capacity, Paresthesias, Ataxia Pernicious Anemia A comprehensive physical examination should be performed, seeking clinical clues to possible underlying physiological and pathological disorders. A neurological evaluation should include a mental status examination (to identify neurodegenerative disease and motor testing (Parkinson’s disease or multiple strokes), sensory testing (peripheral neuropathy), and pupillary size (Horner’s syndrome) Evaluation and Management of Orthostatic Hypotension ; American Family Physician Volume 84, Number 5 ; September 1, 2011

30 Ancillary Tests / Imaging
Conditions Suspected BASIC METABOLIC PROFILE BUN & Cr Intravascular volume depletion Electrolytes Electrolyte abnormalities from vomiting or diarrhea, or as cause of cardiac conduction abnormalities; clues to adrenal insufficiency (Dec Na & K) Serum Glucose Hyperglycemia IMAGING CT +/- MRI Neurodegenerative disease, stroke COMPLETE BLOOD COUNT White Count Infections H&H Anemia Platelet Count Sepsis ECHO CHF, Structural heart disease EKG Cardiac arrhythmia, myocardial infarction MORNING SERUM CORTISOL LEVELS Adrenal insufficiency SERUM VITAMIN B12 LEVEL Neuropathy from vitamin B12 deficiency TELEMETRY MONITORING Cardiac arrhythmia RPR/ VDRL Syphilis laboratory tests should be obtained based on the results of these assessments. These may include hemoglobin and hematocrit levels to evaluate for anemia; blood electrolytes, urea nitrogen, and creatinine to assess for dehydration; a rapid plasma reagin (RPR) test for syphilis; and a glucose tolerance test for diabetes. Evaluation and Management of Orthostatic Hypotension ; American Family Physician Volume 84, Number 5 ; September 1, 2011

31 Head Up-Tilt (HUT) Indications for Head-up tilt testing
High probability of OH despite an initial negative evaluation (e.g., PD) Patients with significant motor impairment that precludes them from having standing vital signs obtained. Lahrmann H.; Cortelli P.; Hilz M.; Mathias C.J.; Struhal W.; Tassinari M. EFNS guidelines on the diagnosis and management of orthostatic hypotension. Eur. J. Neurol. 2006, 13, To monitor the course of an autonomic disorder and its response to therapy. Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. Am J Med 2007 Oct; 120 (10):

32 Procedure of HUT Perform tilt-table testing in a quiet room with a temperature of 68°F to 75°F. The patient should rest while supine for 5 minutes before testing is started. Continuous HR monitoring and blood pressure monitoring at regular intervals. The table should be slowly elevated to an angle between 60 to 80 * for 3 minutes. The test is considered Positive if systolic blood pressure falls 20 mm Hg below baseline or if diastolic blood pressure falls 10 mm Hg below baseline. Measurement of plasma noradrenaline levels while supine and upright may be of some value. If symptoms occur during testing, the patient should be returned to the supine position immediately.

33 Evaluation The procedure is generally considered safe, but serious adverse events such as syncope and arrhythmias have been reported.

34 Responses to Head-Up Tilt Table Testing
Condition Response Normal HR increases by 10 to 15 beats per minute DBP increases by 10 mm Hg or more Dysautonomia No increase in heart rate Immediate and continuing drop in systolic and diastolic blood pressure Neurocardiogenic syncope ( Occurs after 10 minutes or more of testing ) Bradycardia Symptomatic, sudden drop in blood pressure Orthostatic hypotension SBP decreases by 20 mm Hg or more or DBP decreases by 10 mm Hg or more Postural orthostatic tachycardia syndrome Heart rate increases by at least 30 beats/ minute Persistent tachycardia of more than 120 beats/ minute

35 Orthostatic Hypotension
Management of Orthostatic Hypotension

36 GOALS DO NOT CHASE THE NUMBERS ….!!!!
Goals should be directed towards : Ameliorating symptoms Relieving orthostatic symptoms Improving the patient’s functional status Improving standing time Reducing the risk of complications. Improving OH without excessive hypertension Correcting any underlying cause No specific or single treatment is currently available that achieves all these goals. Drugs alone are never completely adequate. Therapies primarily consist of a combination of vasoconstrictor drugs, volume expansion, compression garments, and postural adjustment. Education about orthostatic stressors and warning symptoms empowers the patient to adopt easy lifestyle changes to minimize and handle orthostatic stress. .

37 Supine Hypertension Supine hypertension is a problem.
Resulting from medication and/or being part of the disease. 24 h measurement of BP is best if diagnosis uncertain. After starting a new therapy. Patients may self-monitor BP, daily at about the same time, and when they experience symptoms. Pressor medications should be avoided after 6pm and the bed head elevated (20–30 cm). On occasion, short acting antihypertensive drugs may be considered (e.g. Nitro-glycerine sublingual). Lahrmann H.; Cortelli P.; Hilz M.; Mathias C.J.; Struhal W.; Tassinari M. EFNS guidelines on the diagnosis and management of orthostatic hypotension. Eur. J. Neurol. 2006, 13, .

38 Management Pneumonic A B C D E F A  Abdominal compression
B  Bolus of water B  Bed up C  Countermaneuvers D  Drugs E  Education E  Exercise F  Fluids and salt The alphabetic order is not meant to represent a sequential approach to management, but rather to facilitate consideration of all the available treatments. .

39 Non-Pharmacologic Treatment
A : Abdominal and Lower Extremity Binders Podoleanu C, Maggi R, Brignole M, et al. Lower limb and abdominal compression bandages prevent progressive orthostatic hypotension in elderly persons: a randomized single-blind controlled study. J Am Coll Cardiol. 2006;48(7): B : Upto 1 to 2 L of fluid/ day to balance expected 24-hour urine losses  increase standing SBP by > 20 mm hg for approx. two hours. Shannon JR, Diedrich A, Biaggioni I, et al. Water drinking as a treatment for orthostatic syndromes. Am J Med. 2002;112(5): B : Raise the head of the bed 10 to 20 degrees (~ 4 inches )  pts with autonomic failure and supine hypertension  reduce nocturnal hypertension and diuresis  helps restore morning blood pressure upon standing. Van Lieshout JJ, Ten Harkel AD, Wieling W. Fludrocortisone and sleeping in the head-up position limit the postural decrease in cardiac output in autonomic failure. Clin Auton Res 2000; 10:35–42. C : - Isometric exercises involving the arms, legs, and abdominal muscles. - Active standing with legs crossed, with or without leaning forward. Low PA, Singer W. Management of neurogenic orthostatic hypotension: an update. Lancet Neurol. 2008;7(5): In conditions in which there is adrenergic denervation of vascular beds, there is an increase in vascular capacitance and peripheral venous pooling. Compression of capacitance beds (ie, the legs and abdomen) improves orthostatic during violent aircraft maneuvers) inflated to 20 mm Hg—an increase of about 17/8 mm Hg. Higher gravity-suit pressures had a greater effect. In practical terms, the binder should be tight enough to exert gentle pressure. It should be put on before rising from bed in the morning and taken off when lying supine, to avoid supine hypertension. Advantages are that a binder’s effects are immediate, its benefits can be easily assessed, and it can be used on an as-needed basis by patients who need it only during periods of prolonged orthostatic stress. Binders are also easy to fit and are available in most sporting good stores and on the Web (try searching for “abdominal binder”). Physical countermaneuvers involve isometrically contracting the muscles below the waist for about 30 seconds at a time, which reduces venous capacitance, increases total peripheral, resistance, and augments venous return to the heart.These countermeasures can help maintain blood pressure during daily activities and should be considered at the first symptoms of orthostatic intolerance and in situations of orthostatic stress (eg, standing for prolonged periods). Rapidly drinking two 8-oz (500-mL) glasses of cold water helps expand plasma volume. It also, within a few minutes, elicits a significant pressor effect that is in part norepinephrine mediated, increasing the standing systolic blood pressure by more than 20 mm Hg for about 2 hours and improving symptoms and orthostatic endurance. This easy technique can be used when prolonged standing is expected (eg, shopping). The head of the bed of a patient with orthostatic hypotension should be elevated by 10 to 20 degrees or 4 inches (10 cm) to decrease nocturnal hypertension and nocturnal diuresis. During the day, adequate orthostatic stress, ie, upright activity, should be maintained. If patients are repeatedly tilted up, their orthostatic hypotension is gradually attenuated, presumably by increasing venomotor tone. The head of the bed of a patient with orthostatic hypotension should be elevated by 10 to 20 degrees or 4 inches (10 cm) to decrease nocturnal hypertension and nocturnal diuresis.21 During the day, adequate orthostatic stress, ie, upright activity, should be maintained. If patients are repeatedly tilted up, their orthostatic hypotension is gradually attenuated, presumably by increasing venomotor tone. .

40 Non-Pharmacologic Treatment
D : D/c culprit medications  If unable to D/C culprit medications; advise patient to take at bedtime such as anti-hypertensives. Freeman R. Clinical practice. Neurogenic orthostatic hypotension. N Engl J Med. 2008;358(6): E : Education Symptom diary  avoid identified precipitating factors Avoid large carbohydrate-rich meals (to prevent postprandial hypotension) Limit alcohol intake Lahrmann H.; Cortelli P.; Hilz M.; Mathias C.J.; Struhal W.; Tassinari M. EFNS guidelines on the diagnosis and management of orthostatic hypotension. Eur. J. Neurol. 2006, 13, E : Exercise programs improves conditioning. Squatting has been used to alleviate symptomatic OH Toe raises, thigh contractions, and bending over at the waist are recommended Low PA, Singer W. Management of neurogenic orthostatic hypotension: an update. Lancet Neurol. 2008;7(5): .

41 Non-Pharmacologic Treatment
F : Fluid & Salts Upto 1 to 2 L of fluid/ day  increase standing SBP by > 20 mm hg. Shannon JR, Diedrich A, Biaggioni I, et al. Water drinking as a treatment for orthostatic syndromes. Am J Med. 2002;112(5): Sodium supplementation  adding extra salt to food or taking ~ 1 to 2 gms of salt tablets TID. A 24-hour urine sodium level can aid in treatment. Value of <170 mmol per 24 hours, should be placed on 1 to 2 g of supplemental sodium three times daily Reevaluate in one to two weeks Goal of raising urine sodium to between 150 and 200 meq. Patients should be monitored for weight gain and edema. Low PA, Singer W. Management of neurogenic orthostatic hypotension: an update. Lancet Neurol. 2008;7(5): .

42 FLUDROCORTISONE A synthetic mineralocorticoid.
Reducing salt loss and expanding blood volume. Hussain RM, McIntosh SJ, Lawson J, Kenny RA. Fludrocortisone in the treatment of hypotensive disorders in the elderly. Heart 1996; 76:507–509. Sensitization of alpha-adrenoceptors. First line therapy (monotherapy) approved by FDA in 1955. Initial dose is 0.1 mg per day with increments of 0.1 mg every week. May be increased to 0.4 to 0.6 mg/day in refractory cases. Dose titration needed until : Resolution of the symptoms OR Patient develops trace peripheral edema OR Weight gain of 4 to 8 lbs OR The maximum dose of 1 mg per day is reached. Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. Am J Med 2007 Oct; 120 (10): This medication is helpful when plasma volume fails to adequately increase with salt supplementation31 and for patients who cannot ingest enough salt or do not respond adequately to midodrine. If the patient gains 3 to 5 pounds (1.2–2.3 kg) and develops mild dependent edema, you can infer that the plasma volume has expanded adequately. .

43 FLUDROCORTISONE After oral administration, Peak plasma levels ~ 45 min
Elimination half-life ~ 7 h. Adverse effects include : Headache Supine hypertension Congestive heart failure Hypokalemia Dose-dependent In one study, hypokalemia in 24% of patients with mean onset at 8 months. Hussain RM, McIntosh SJ, Lawson J, Kenny RA. Fludrocortisone in the treatment of hypotensive disorders in the elderly [published correction appears in Heart. 1997;77(3):294]. Heart. 1996;76(6): .

44 MIDODRINE Prodrug with an active metabolite, Desglymidodrine.
Peripheral selective alpha-1 adrenergic agonist; cause vasoconstriction. Absolute bioavailability ~ 93% The elimination half-life ~ 2–3 h Duration of action ~ 4 h. First approved by FDA in 1996. Significantly increase systolic BP  avoid last dose after 6 pm to avoid supine HTN. Improve symptoms in patient with Neurogenic Hypotension. Synergistic effect when combined with fludrocortisone. Starting dose = 2.5 mg 3 times per day. Then 2.5 mg weekly increments until a max. of 10 mg TID is reached. Before arising from bed in morning ---- Before lunch ---- Mid-afternoon Vasoconstrictors such as midodrine are ineffective when plasma volume is reduced. .

45 MIDODRINE Adverse effects : Supine Hypertension (25%)
Piloerection/ goose bumps (13%) Pruritis (scalp-10% & general- 2%) Paresthesia (9%) Contraindications : Coronary Artery Disease Urinary Retention (worsens urinary retention) Thyrotoxicosis Acute Renal Failure (Excreted in urine) FDA has issued a recommendation to withdraw midodrine from the market because of a lack of post-approval effectiveness data. U.S. Food and Drug Administration. Drug safety and availability. Midodrine update. September 2010. .

46 PROSTAGLANDIN INHIBITORS
Block the vasodilating effects of prostaglandins  raise the BP in some patients. Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. Am J Med 2007 Oct; 120 (10): In elderly patients, indomethacin should be avoided because of associated confusion. All NSAIDS should be used with caution due to gastrointestinal and renal side effects. .

47 CAFFEINE Adenosine-receptor blocker .
Inhibits adenosine induced vasodilatation by blocking these receptors. Methylxanthine Caffeine Administered in a dose of 200 mg every morning as 2 cups of brewed coffee or by tablet. May attenuate symptoms in some patients. To avoid tolerance and insomnia, caffeine should not be given more then once in the morning. .

48 ERYTHROPOIETIN Exact mechanism of action is unknown
Effect is probably due to increased red cell mass and blood volume. Shown to be effective in a subgroup of patients with anemia and autonomic dysfunction. Hoeldtke RD, Streetan DHP. Treatment of orthostatic hypotension with erythropoietin. N Engl J Med. 1993;329: Principal disadvantage of this drug is the Parenteral route of administration. Serious side effects include: Hypertension Stroke Myocardial infarction .

49 PYRIDOSTIGMINE Cholinesterase inhibitor
Potentiates sympathetic baroreflex pathway. Approved by FDA : Myaesthenia Gravis (1955) Bioterrorism Increase survival after exposure to Soman "nerve gas" poisoning (2003) Off-Label use for Orthostatic Hypotension Used for patients with mild to moderate hypotension due modest pressor effect. Does not aggravate supine hypertension. Enhanced effect when taken with Midodrin 5 mg. Starting Dose : 30 mg TID  increased to 60 mg TID. 180 mg slow release pyridostigmine (Mestinon Timespan) can be taken once a day. Because this pathway is activated primarily during standing, this drug improves orthostatic hypotension and total peripheral resistance without aggravating supine hypertension. Because .

50 PYRIDOSTIGMINE Adverse effects : Loose stools Diaphoresis
Hypersalivation Fasciculations Because this pathway is activated primarily during standing, this drug improves orthostati hypotension and total peripheral resistance without aggravating supine hypertension. Because the pressor effect is modest, it is most adequate for patients with mild to moderate orthostatic hypotension. .

51 OCTREOTIDE Somatostatin Analogue
Inhibits release of gastrointestinal peptides, some of which cause vasodilation. Administered subcutaneously starting with 25–50 mcg. In patients with pure autonomic failures : Reduces postural, post-parandial and exertional hypotension. Does not cause or increase nocturnal hypertension. .

52 OTHER AGENTS CLONIDINE Peripheral – alpha 2-adrenergic agonist
May improve OH in patients with CNS causes of autonomic failure : By promoting peripheral venoconstriction. Thereby increasing venous return to the heart. YOHIMBINE Central –alpha 2-adrenergic antagonist. .

53 Indication for Referral
Referral Specialist Indications Geriatrician Multiple comorbid conditions Failure of standard therapy to alleviate symptoms Complications, including recurrent falls, fracture, functional decline, ischemic events, decreased quality of life Cognitive decline and confusion Frail elderly patients Cardiologist Uncontrolled supine hypertension despite standard therapy Advanced coronary artery disease or severe ischemic symptoms Severe left ventricular diastolic or systolic dysfunction (ejection fraction30%) Recent onset of tachy-/bradyarrhythmia Neurologist Specialized diagnostic testing for autonomic failure Chronic and progressive autonomic failure

54 SUMMARY Regardless of whether OH is symptomatic or asymptomatic, the elderly patient remains at significant risk for future falls, fractures, TIA and MI. The diagnostic evaluation of OH should include a comprehensive history and physical examination, careful blood pressure measurements, and laboratory studies. Goals of treatment in the elderly patient include ameliorating symptoms, correcting any underlying cause, improving the patient’s functional status, and reducing the risk of complications, rather than trying to attain an arbitrary blood pressure goal. .

55 SUMMARY In most cases, treatment begins with nonpharmacological interventions, including withdrawal of offending medications (when feasible), physical maneuvers, compression stockings, increased intake of salt and water, and regular exercise. If nonpharmacological measures fail to improve symptoms, pharmacologic agents should be initiated. Fludrocortisone, midodrine, nonsteroidal anti-inflammatory drugs, caffeine, and erythropoietin have all been used to treat orthostatic hypotension due to autonomic failure. .

56 REFERENCES Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. The Consensus Committee of the Ameri­can Autonomic Society and the American Academy of Neurology. Neurology. 1996;46(5):1470. Ooi WL, Barrett S, Hossain M, Kelley-Gagnon M, Lip­sitz LA. Patterns of orthostatic blood pressure change and their clinical correlates in a frail, elderly population. JAMA. 1997;277(16): Rutan GH, Hermanson B, Bild DE, Kittner SJ, labaw F, Tell GS. Orthostatic hypotension in older adults. The Car­diovascular Health Study. CHS Collaborative Research Group. Hypertension. 1992;19(6 pt 1): Freeman R. Clinical practice. Neurogenic orthostatic hypotension. N Engl J Med. 2008;358(6): Sandroni P, Ahlskog JE, Fealey RD, Low PA. Autonomic involvement in extrapyramidal and cerebellar disorders. Clin Auton Res 1991; 1:147–155. Saito Y, Matsuoka Y, Takahashi A, Ohno Y. Survival of patients with multiple system atrophy. Intern Med 1994; 33:321–325. Uukinen H, Koski K, Laippala P, Kivelä SL. Prognosis of Diastolic and systolic orthostatic hypotension in older Persons. Arch Intern Med 1999; 159:273–280. Davis BR, Langford HG, Blaufox MD, Curb JD, Polk BF, Shulman NB. The association of postural changes in systolic blood pressure and mortality in persons with hypertension: the Hypertension Detection and Follow-up Program experience. Circulation 1987; 75:340–346. .

57 REFERENCES Hoeldtke RD, Streeten DH. Treatment of orthostatic hypotension with erythropoietin. N Engl J Med 1993; 329:611–615. Sarasin FP, Louis-Simonet M, Carballo D, Slama S, Rajeswaran A, Metzger JT, et al. Prospective evaluation of patients with syncope. Am J Med 2001;111:177-84 Biaggioni I, Griffin MR. Orthostatic hypotension-related hospitalizations in the United States. Am J Med Nov;120(11):975-80 Carlson JE. Assessment of orthostatic blood pressure: measurement technique and clinical applications. South Med J. 1999;92(2): Cooke J, Carew S, O’Connor M, Costelloe A, Sheehy T, Lyons D. Sitting and standing blood pressure measure­ments are not accurate for the diagnosis of orthostatic hypotension. QJM. 2009;102(5): Lamarre-Cliche M, Cusson J. The fainting patient: value of the head-upright tilt-table test in adult patients with orthostatic intolerance. CMAJ. 2001;164(3): Jamnadas-Khoda J, Koshy S, Mathias CJ, Muthane UB, Ragothaman M, Dodaballapur SK. Are current recommendations to diagnose orthostatic hypoten­sion in Parkinson’s disease satisfactory? Mov Disord. 2009;24(12): .

58 THANK YOU QUESTIONS ??


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