CE ARTICLE

Orthostatic hypotension in older people Yaelim Lee, RN, MSN (PhD Student) School of Nursing, University of Pennsylvania, Philadelphia, Pennsylvania

Keywords Orthostatic hypotension; postural hypotension; dizziness; older people. Correspondence Yaelim Lee, School of Nursing, University of Pennsylvania, Claire M. Fagin Hall, Philadelphia, PA 19104-4217. Tel: 215-407-3004; E-mail: [email protected] Received: July 2012; accepted: January 2013 doi: 10.1002/2327-6924.12026 To obtain CE credit for this activity, go to www.aanp.org and click on the CE Center. Locate the listing for this article and complete the post-test. Follow the instructions to print your CE certificate. Disclosure The author reports no competing interests.

Abstract Purpose: To enhance awareness of orthostatic hypotension (OH) in older populations, and guide primary care nurse practitioners (NPs) in the assessment and management of patients with OH. Data sources: Electronic data collection was conducted on studies and reviews that were published between 2005 and 2012 in English, and contained information related to the purpose of this article from following databases: PubMed, Scopus, and MEDLINE. Conclusions: OH is a syndrome that is accompanied by unfavorable symptoms such as dizziness, and headaches and can impede the individual’s daily activities and quality of life. The prevalence of OH is higher in older people because of comorbidities, polypharmacy, and physiological changes that occur with aging. OH is diagnosed with serial blood pressure measurements and the primary goal of management is to relieve unfavorable symptoms and enhance patient safety. Pharmacological management is considered when nonpharmacological interventions fail. Implications for practice: OH is not a problem to be taken lightly as it is highly related to the risk of falling and cardiovascular problems, as well as increasing morbidity and mortality rates. NPs can contribute to improving the quality of life for older adults and reducing adverse consequences by understanding OH and adequately managing it.

Orthostatic hypotension (OH) is a prevalent problem among older people and is often inadequately evaluated and treated (Feldstein & Weder, 2012). According to diagnostic criteria developed by the Consensus Committee of the American Autonomic Society and the American Academy of Neurology in 1996, diagnosis of OH can be made with a decrease in systolic blood pressure (SBP) of 20 mmHg or a decrease in diastolic blood pressure (DBP) of 10 mmHg within 3 min of standing (Fedorowski, Stavenow et al., 2010; Feldstein & Weder, 2012; Figueroa, Basford, & Low, 2010; Gupta & Lipsitz, 2007). In 2004, the United States Nationwide Inpatient Sample showed that 36 hospitalizations per 100,000 adults occurred because of OH; furthermore, the incidence of OH increases with age (Shibao, Grijalva, Raj, Biaggioni, & Griffin, 2007). This trend can be explained by understanding the etiology of OH and the physiological changes associated with normal aging (Gupta & Lipsitz, 2007). Many studies have shown a strong link between OH and common chronic diseases such as hypertension and heart problems, as well as neurodegenerative

diseases such as Parkinson’s disease and autonomic neuropathies (Fedorowski, Stavenow et al., 2010; Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007; Shibao et al., 2007). Older people have a higher incidence of these chronic diseases (Figueroa et al., 2010). In addition, the physiological change of failure to maintain adequate blood pressure with postural change, which occurs normally with aging, makes older people more prone to OH (Feldstein & Weder, 2012; Gupta & Lipsitz, 2007). This becomes more important for the institutionalized population. Many surveys have shown that 10%–68% of older individuals living in institutions have OH, while 6%–33.7% living in the community have OH (Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007; Kobayashi & Yamada, 2011; Shibao et al., 2007). The common symptoms of OH predispose older people to have a high risk of falling, which starts the vicious circle of injury, fracture, disability, and ensuing frailty (Gupta & Lipsitz, 2007; Shibao et al., 2007; Xue, 2011). Moreover, OH has been proven to increase morbidity and

C 2013 The Author(s) Journal of the American Association of Nurse Practitioners 25 (2013) 451–458 

 C 2013 American Association of Nurse Practitioners

451

Orthostatic hypotension in older people

mortality rates, and to be a risk factor for cardiovascular problems, including myocardial ischemia, heart failure, and stroke (Fedorowski, Stavenow et al., 2010; Feldstein & Weder, 2012; Gupta & Lipsitz, 2007; Jones et al., 2012; Kobayashi & Yamada, 2011; Shibao et al., 2007). It is also a mortality indicator for patients with end-stage renal disease (Shibao et al., 2007). In a Rotterdam study, patients with OH had a 20%–30% higher incidence of cardiovascular disease or stroke in a 6-year follow-up (Feldstein & Weder, 2012). In addition, the Honolulu Heart Program found a higher mortality rate in patients with OH at a 4-year follow-up; the Atherosclerosis Risk in Communities study showed an increased risk of ischemic stroke in patients with OH at a 7.9-year follow-up (Feldstein & Weder, 2012). Considering that OH is a modifiable risk factor for many adverse consequences, including falls, and despite numerous studies that emphasize the clinical importance of OH, the condition is generally not checked in the clinical setting unless the patient complains of possible symptoms (Allan, Ballard, Rowan, & Kenny, 2009; Feldstein & Weder, 2012). Taking into account the many prospective studies using data from the Malmo Prevention Project, which showed a close correlation between asymptomatic OH and a higher risk of cardiovascular problems, including coronary events, heart failure, and atrial fibrillation, it is reasonable to recommend screening for OH, even in asymptomatic individuals, to predict any risk of future ¨ problems (Fedorowski, Engstrom, Hedblad, & Melander, 2010; Fedorowski, Stavenow et al., 2010; Raj, 2010).

Physiology of blood pressure regulation Changes in blood pressure occur directly from cardiac output, heart rate, stroke volume, and vascular resistance (Gupta & Lipsitz, 2007). With orthostatic change, approximately 500–700 mL of blood moves to the lower extremities, the splanchnic region, and the pulmonary circulation system (Feldstein & Weder, 2012). Fluid in the lower extremities moves from the blood vessels to interstitial space, decreasing the venous return to the heart, resulting in insufficient left ventricular filling and decreased cardiac stroke volume, resulting in a decrease in SBP and DBP (Feldstein & Weder, 2012; Figueroa et al., 2010). The change in blood pressure activates baroreceptors located in the carotid sinus, aortic arch, heart, and lungs, and increases the sympathetic nervous system while decreasing parasympathetic tone (Feldstein & Weder, 2012; Figueroa et al., 2010). Together, these functions help to maintain cardiac output by raising the heart rate, 10–25 beats per minute, and increasing venous return by constricting peripheral vascular resistance 452

Y. Lee

(Feldstein & Weder, 2012; Figueroa et al., 2010; Medow et al., 2008). The renin–angiotensin–aldosterone system (RAAS) becomes activated in response to the sympathetic nervous system, which contributes to vasoconstriction, while other compensations including venoarteriolar reflex and myogenic response, occur to perfuse blood flow to the skin, muscle, and adipose tissue (Feldstein & Weder, 2012).

Pathogenesis Any impairment in the normal compensation mechanism of blood pressure may contribute to a failure to maintain adequate blood pressure after standing up (Gupta & Lipsitz, 2007). OH can be divided into acute and chronic OH, depending on the symptoms and etiology (Gupta & Lipsitz, 2007). While acute OH is mostly symptomatic and caused by secondary problems, including medication, fluid or blood deficiency, and adrenal insufficiency, most chronic OH is asymptomatic and caused by primary problems, including autonomic nervous system dysfunction and altered regulatory mechanism (Gupta & Lipsitz, 2007).

Health condition Hypovolemic status, including dehydration from burns, diarrhea, vomiting, or hemorrhage, may also cause a person to develop OH (Feldstein & Weder, 2012; Gupta & Lipsitz, 2007). Patients with both OH and anemia may have worse symptoms as a result of fewer blood cells, causing a low oxygen supply to the brain (Feldstein & Weder, 2012; Gupta & Lipsitz, 2007). Some cardiovascular problems that can cause OH are hypertension, heart failure, arrhythmia, aortic stenosis, myocardial infarction, diastolic dysfunction, and a history of carotid endarterectomy (Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007). Neurological diseases such as Parkinson’s, Alzheimer’s, Guillain–Barre syndrome, dementia with Lewy bodies, and atrophy of multiple systems may contribute to OH by causing autonomic failure; endocrinological problems, including abnormal regulation of aldosterone, adrenal insufficiency, and diabetes insipidus, can cause circulating fluid imbalance. In addition, alcohol and marijuana abuse, pregnancy, uremia, autoimmune diseases, and porphyria are related to OH (Feldstein & Weder, 2012). A study conducted on 108 hospitalized patients over the age of 60 showed that the incidence of OH increases with long bed rest, and that a sedentary lifestyle contributes to having OH (Feldstein & Weder, 2012; Gorelik et al., 2009).

Orthostatic hypotension in older people

Y. Lee

Medication Many medications can cause OH, particularly antihypertensive drugs (Feldstein & Weder, 2012). However, which antihypertensive drug has a higher risk of OH is inconsistent among studies. Nevertheless, many studies have shown that patients on diuretics (hydrochlorothiazide, furosemide), alpha-blockers (terazosin), and nondihydropyridine calcium channel blockers have a higher risk of OH (Feldstein & Weder, 2012; Figueroa et al., 2010; Poon & Braun, 2005). Nifedipine is especially known for its action of increasing sodium excretion at night, which causes morning OH (Feldstein & Weder, 2012). Other medications, including vasodilators, antiparkinson agents (levodopa, bromocriptine), antidepressants (tricyclic antidepressants, trazodone, paroxetine, venlafaxine, monoamine oxidase inhibitors), insulin, betablockers, angiotensin-converting enzyme inhibitors, antipsychotics (chlorpromazine, quetiapine), medications, which can cause autonomic neuropathy (amiodarone, vincristine, cisplatin), phosphodiesterase type 5 inhibitors (sildenafil), nitroglycerin, narcotics (morphine), and sedatives, can all cause OH (Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006).

with chronic asymptomatic OH, as they age, can become symptomatic with various changes, including altered posture, new medications or health conditions, stress, or fluid and electrolyte imbalance (Gupta & Lipsitz, 2007).

Clinical presentation The most common symptoms across age groups are related to cerebral hypoperfusion (dizziness, lightheadedness, weakness, syncope, difficulty thinking, and headache) and compensation from the autonomic system (palpitation, chest pain, low back pain, nausea, tremor, cold extremities; Figueroa et al., 2010; Gupta & Lipsitz, 2007; Kobayashi & Yamada, 2011). However, older people may present with additional atypical symptoms, including disturbed speech, visual changes, falling, confusion, and impaired cognition, because of comorbid conditions and polypharmacy (Gupta & Lipsitz, 2007). Therefore, when facing older people with these symptoms, especially those with a history of frequent falls, thorough history taking and precise blood pressure measurement are crucial (Figueroa et al., 2010; Gupta & Lipsitz, 2007).

Diagnosis

Age-related physiological change Several age-related changes occur that may contribute to a failure to respond well to alterations in blood pressure (Gupta & Lipsitz, 2007). With aging, the body becomes less sensitive to the baroreflex, decreasing vasoconstrictor responsiveness to sympathetic stimuli and failing to achieve a normal decrease in parasympathetic activity upon standing (Feldstein & Weder, 2012; Gupta & Lipsitz, 2007; Kobayashi & Yamada, 2011). A decrease in the normal function of the RAAS and kidneys when it comes to maintenance of fluid balance, decreased thirst, and inadequate water intake in older people contribute to OH as well (Gupta & Lipsitz, 2007; Kobayashi & Yamada, 2011). In addition, a stiff and less compliant heart makes diastolic filling more difficult and less responsive to preload, while an increase in supine blood pressure with aging increases nocturnal urination, which contributes to OH (Gupta & Lipsitz, 2007). Moreover, deterioration of the musculoskeletal system makes older people less mobile and impairs sufficient venous return (Kobayashi & Yamada, 2011). In addition to coexisting medical conditions, these age-related physiological changes make older people more prone to OH (Figueroa et al., 2010; Gupta & Lipsitz, 2007). The prevalence of asymptomatic OH is reported to be 56%–89% (Kobayashi & Yamada, 2011). Even people

A comprehensive history and physical examination of the patient, including reviewing coexisting medical problems and the medication list, are important for a better understanding of the etiology of OH and for planning treatment (Gupta & Lipsitz, 2007). Good assessment is also important in asymptomatic OH patients, as they may still be at risk of becoming symptomatic in distressed situations. Figure 1 provides a quick guide for assessing and managing patients with OH. OH is traditionally defined by the measurement of blood pressure while lying down for at least 5 min, followed by measurement at 1 min and 3 min after standing (Feldstein & Weder, 2012; Gupta & Lipsitz, 2007). However, the timing of blood pressure measurement after standing up varies slightly depending on whether the care providers recognize progressive and delayed types of ¨ et al., 2010; Gehrking, Hines, OH (Fedorowski, Engstrom Benrud-Larson, Opher-Gehrking, & Low, 2005; Gibbons & Freeman, 2006; Kobayashi & Yamada, 2011). In Gibbons and Freeman’s 2006 study, 39% of the participants had blood pressure falls after 10 min of head-up tilt, while another study showed that the decrease in SBP was greater 7 min after standing than after 3 min, which suggests the necessity of additional later measurements after the usual measurement (Feldstein & Weder, 2012). Understanding the possibility of delayed OH is important, as 453

Orthostatic hypotension in older people

Y. Lee

Clinical Presentation -Cerebral hypoperfusion: Dizziness, light-headedness, weakness, syncope, difficulty thinking, and headache -Compensation from the autonomic system: Palpitation, chest pain, low back pain, nausea, tremor, cold extremities -Atypical symptoms in older people: Disturbed speech, visual changes, falling, confusion, and impaired cognition

Assessment -Measurement of BP and HR: While lying down for at least five minutes, then one minute and three minutes after standing

Diagnosis of OH -Decrease in SBP of 20mmHg or 10mmHg of DBP within three minutes of standing (Consensus Committee of the American Autonomic Society and the American Academy of Neurology, 1996) -Additional: Change in HR below or over 10-25 beats/min

Assessment for possible causes 1) Health condition -Hypovolemic: Dehydration, burns, diarrhea, vomiting, or hemorrhage -CV: HTN, HF, arrhythmia, aortic stenosis, MI, diastolic dysfunction, carotid endarterectomy -Neurologic: Parkinson’s, Alzheimer’s, Guillain-Barre syndrome, dementia with Lewy bodies, atrophy of multiple systems -Endocrinologic: Abnormal regulation of aldosterone, adrenal insufficiency, diabetes insipidus -Others: Alcohol abuse, marijuana abuse, pregnancy, uremia, autoimmune diseases, porphyria, sedentary lifestyle

Abnormal

Thorough BP measurement -Various measurements throughout the day/on different days: Before and after meals, after medication, before bed -Ambulatory BP monitoring

Normal

Referral - Cardiologist: When advanced diagnostic tests are needed. With failure of standard therapy or advanced cardiac disease and symptoms -Neurologist: Advanced neurological diagnostic tests are required or with refractory autonomic failure - Physical therapist: For instruction on non-pharmacological strategies to relieve OH symptoms

2) Medication Antihypertensives, vasodilators, antiparkinson agents, antidepressants, insulin, antipsychotics (chlorpromazine, quetiapine), medication for autonomic neuropathy (amiodarone, vincristine, cisplatin), phosphodiesterase type 5 inhibitors (sildenafil), nitroglycerin, narcotics (morphine), other sedatives

Clinical management Goal: Do not treat number, but treat symptoms and underlying cause Increase patient’s standing BP while keeping the supine BP stable 1) Non-pharmacological -Adjust medication, maintain sufficient body fluid -Promote venous return: Countermaneuvers (e.g., contracting lower extremities), compression stockings, abdominal binders -Exercise: Isotonic exercise>Isometric exercise. Swimming, recumbent biking, rowing, tilt-up exercise -Prevent supine hypertension: Elevating the head of the bed to 10–20 degrees at night. Bedtime snack -Prevent postprandial hypotension: Avoid large, high-carbohydrate meals. Small meal and coffee for breakfast -Others: Avoid alcohol intake, exposure to heat (hot food, drink, bath, weather), sudden change in position, sedentary lifestyle 2) Pharmacological -Fludrocortisone: For patients who cannot ingest enough water and sodium. Initial dose 0.1mg PO daily (Max: 1mg PO daily) -Pyridostigmine: For patients with mild symptoms. Initial dose 30mg PO BID or TID (Max: 60mg PO TID) -Midodrine: For patients with severe symptoms. Initial dose: 2.5mg PO TID (Max: 10mg PO TID) -NSAIDs: Special caution needed for older people with neurological adverse effect -Others: Caffeine, erythropoietin, desmopressin, octreotide, clonidine, yohimbine, vitamin B12, fluoxetine, venlafaxine, and pyridostigmine BP = blood pressure; HR = heart rate; SBP = systolic blood pressure; DBP = diastolic blood pressure; HTN = hypertension; HF = heart failure; MI = myocardial infarction; OH = orthostatic hypotension; PO = by mouth; BID = twice daily; TID = three times daily. This figure illustrates clinical pathway for patients with orthostatic hypotension.

Figure 1 Clinical protocol for orthostatic hypotension.

454

Y. Lee

it may indicate further impairment of compensatory reflex than typical OH (Gehrking et al., 2005). Various measurements throughout the day, including before and after meals, after medication, and before bed, or ambulatory blood pressure monitoring and measurements on different days, may be needed for patients with symptoms but normal blood pressure, or for differentiating between OH and postprandial hypotension (Feldstein & Weder, 2012; Gupta & Lipsitz, 2007). For those with unexplained recurrent syncope or suspected of neurocardiogenic syncope, OH can be diagnosed when a head-up tilt test is positive to an angle between 60◦ and 80◦ while standing for 3 min (Figueroa et al., 2010; Grubb, 2005; Moya et al., 2009; Vetta et al., 2009). In addition, measuring heart rate before and after standing is helpful; an increase in heart rate of less than 10 beats/min indicates baroreflex impairment, while an increase of more than 20 beats/min implies volume deficiency or orthostatic intolerance (Gupta & Lipsitz, 2007).

Clinical management The management goal of OH is to relieve unfavorable symptoms by increasing the patient’s standing blood pressure while keeping the supine blood pressure stable (Figueroa et al., 2010; Mansoor, 2006). This should not target the blood pressure level, but rather the individualized symptoms, and treat the underlying cause (Figueroa et al., 2010; Gupta & Lipsitz, 2007). A nonpharmacological approach is most frequently attempted first, after which a combination with pharmacological treatment is tried (Figueroa et al., 2010; Gupta & Lipsitz, 2007).

Nonpharmacological treatment Adjusting medication. As a first step, eliminating unnecessary medication, especially those known to affect blood pressure; reevaluating dosages; and treating other medical conditions that can exacerbate the symptoms should be carefully considered (Figueroa et al., 2010; Gupta & Lipsitz, 2007). Maintaining sufficient body fluid. If OH occurs because of insufficient body fluid, intake of additional fluid and sodium is necessary (Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006). Maintaining a urine output level of 1.5–2 L/24 h through an intake of eight 8-ounce servings of water daily and 10–20 g of salt is recommended if not contraindicated for other health conditions (Figueroa et al., 2010; Gupta & Lipsitz, 2007). In addition, drinking two glasses of cold water can rapidly increase blood pressure by inducing the pressor reflex, which stimulates the sympathetic nervous system (Feldstein & Weder, 2012; Figueroa et al., 2010).

Orthostatic hypotension in older people

Promoting venous return. Promoting venous return to the heart with counter maneuvers, such as contracting the muscles of the lower extremities, for about 30 s may be helpful (Figueroa et al., 2010; Gupta & Lipsitz, 2007). This method includes pointing the toes and feet up before standing up, crossing the legs with resistance, contracting the thigh muscles, bending the waist, and elevating the legs (Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006). Using appliances such as compression stockings and abdominal binders is also useful. Abdominal binders have been shown to be more effective than compression stockings, accounting for 20%–30% of total blood volume, using 15–20 mmHg of pressure, SBP increased 11 mmHg, while DBP increased 6 mmHg (Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007; Logan & Witham, 2012). It is important to note that these appliances should be removed during sleep in order to prevent supine hypertension (Figueroa et al., 2010). Exercise. Exercise in older adults has been shown to help overcome OH through various benefits, including enhancing cerebral blood perfusion (Franke, Allbee, & Spencer, 2006). Isotonic exercise is recommended over isometric exercise, as isometrics can impair venous return when patients hold their breath and engage in straining (Figueroa et al., 2010). For example, repetitively lifting light weights (isotonic) is recommended over holding weights in a fixed position (isometric; Figueroa et al., 2010). Exercises that can be done in a sitting or supine position, such as swimming, recumbent biking, and rowing, are recommended (Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006). In addition, tilt-up exercises can be taught to patients by physical therapists to enhance venomotor tone; such exercises can begin very simply with the patient leaning against the wall and holding an upright position (Feldstein & Weder, 2012; Figueroa et al., 2010). Preventing supine hypertension. Many patients with OH, as well as those on medication to treat OH, may have supine hypertension, increasing blood pressure during sleep and causing nocturia, which may aggravate morning OH (Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006). Elevating the head of the bed to 10◦ –20◦ helps to prevent fluid loss throughout the night by keeping the RAAS activated, thereby contributing to maintaining adequate fluid volume for morning ambulation (Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006). Preventing postprandial hypotension. Older people have been shown to be more prone to postprandial hypotension than younger adults (Abdel-Rahman, 2012). Because postprandial hypotension may aggravate OH, large, high-carbohydrate meals should be avoided 455

Orthostatic hypotension in older people

in symptomatic patients (Figueroa et al., 2010; Mansoor, 2006). However, postprandial hypotension may be inversely used for nocturnal hypertension by having a bedtime snack to decrease blood pressure at night (Figueroa et al., 2010). Patients experiencing worse OH symptoms in the morning may try eating small meals to prevent postprandial hypotension; drinking a cup of coffee to induce a sympathetic effect also may be helpful (Figueroa et al., 2010; Gupta & Lipsitz, 2007).

Treating for combined hypertension and OH. In older people it is common to have both hypertension and OH, and this combination can pose a challenge to healthcare providers (Lee, Donegan, & Moore, 2005). Although, there is no clear management strategy for these people, it is suggested that some antihypertensive medications, such as alpha-blockers be avoided, as they are more likely to induce OH (Coutaz, Lglesias, & Morisod, 2012; Lee et al., 2005; Poon & Braun, 2005). Administering antihypertensive medications alongside the strategies mentioned that promote venous return may also be helpful in preventing OH (Lee et al., 2005). Other measures. Some other considerations for preventing OH include abstaining from alcohol, hot food, and hot drinks, as well as avoiding exposure to heat, such as hot weather and hot baths (Figueroa et al., 2010; Gupta & Lipsitz, 2007). Avoiding a sudden change in blood pressure by “starting slow and low” is a basic concept to consider in preventing OH symptoms, especially for less active individuals or those on long bed rest (Gupta & Lipsitz, 2007; Mansoor, 2006).

Pharmacological treatment Pharmacological treatment is usually reserved for patients with symptomatic OH who fail to achieve symptom relief with nonpharmacological interventions (Gupta & Lipsitz, 2007; Mansoor, 2006). Fludrocortisone. Individuals with OH from hypovolemia who cannot ingest enough water and sodium can benefit from fludrocortisone, which is a synthetic mineralocorticoid that increases vascular alpha adrenoceptor sensitivity and reserves sodium and water (Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006). The initial dosage is 0.1 mg daily; this may be increased up to 1 mg daily with careful consideration given to common side effects such as supine hypertension, hypokalemia, heart failure, headache, and fluid retention (Figueroa et al., 2010; Gupta & Lipsitz, 2007; Mansoor, 2006). Frequent monitoring of serum potassium, weight change, and edema is needed with this medication (Figueroa et al., 2010).

456

Y. Lee

Pyridostigmine. For those with mild OH, pyridostigmine may be considered, with an initial dosage of 30 mg twice or three times daily that can be increased to 60 mg three times daily (Figueroa et al., 2010). This is a cholinesterase inhibitor that improves neurotransmission in sympathetic baroreflex passage, with the additional benefit of having low risk of causing supine hypertension (Figueroa et al., 2010). However, the effect of this medication is mild, and an additional low dose of midodrine 5 mg may be required in order to achieve effectiveness (Figueroa et al., 2010). The main side effects of this drug are cholinergic, including abdominal discomfort and diarrhea (Figueroa et al., 2010). Midodrine. For patients experiencing severe OH, midodrine, which is an alpha-1 agonist, should be considered at an initial dose of 2.5 mg three times daily; this may be increased weekly to a maximum dose of 10 mg three times daily (Figueroa et al., 2010; Gupta & Lipsitz, 2007). This is a Food and Drug Administration (FDA)approved drug for hypotension management (Mansoor, 2006) that causes blood pressure elevation by increasing peripheral vascular resistance, thereby stimulating aortic and carotid baroreceptors (Lamarre-Cliche, Souich, Champlain, & Larochelle, 2008). Because it has a quick onset of action and short duration, taking the morning dose before getting out of bed is useful (Figueroa et al., 2010). A midday dose can be taken before lunch, given its maximal effect is within 60 min after intake, to prevent postprandial OH (Figueroa et al., 2010; Mansoor, 2006). The last dose of the day can be taken midafternoon to prevent nocturnal hypertension (Figueroa et al., 2010). Common side effects of this medication are supine hypertension, piloerection, pruritus, and paresthesia, especially of the scalp (Figueroa et al., 2010; Gupta & Lipsitz, 2007). Avoid this medication in patients with coronary artery disease, congestive heart failure, thyrotoxicosis, urinary retention, or acute renal failure (Gupta & Lipsitz, 2007; Mansoor, 2006). Nonsteroidal anti-inflammatory (NSAIDs). By using medications, which

drugs

impede the vasodilation effect of prostaglandin, including indomethacin and other NSAIDs, blood pressure can be increased (Gupta & Lipsitz, 2007). However, special caution is needed for older people, as both indomethacin and NSAIDs are known to be linked with adverse neurological effects like delirium in this population (Gupta & Lipsitz, 2007). Other medications. Some other medications to consider are caffeine, erythropoietin, desmopressin, octreotide, clonidine, yohimbine, vitamin B12, fluoxetine, venlafaxine, and pyridostigmine (Gupta & Lipsitz, 2007; Logan & Witham, 2012; Mansoor, 2006). The effects and

Orthostatic hypotension in older people

Y. Lee

safety of these medications are still controversial, and further studies are required (Mansoor, 2006).

Referral Referral for nursing care is essential, as OH care starts from correcting the modifiable factors that can cause OH, such as dehydration or the administering of medication (Figueroa et al., 2010; Gupta & Lipsitz, 2007). Because older people often present atypical symptoms with OH, nurses’ reports and assessments are helpful, especially when faced with a conditional change or recurrent unknown falls (Gray-Miceli, Ratcliffe, Liu, Wantland, & Johnson, 2005). Referral to a cardiologist is needed for a failure with various OH treatment attempts: advanced cardiac disease and symptoms, including severe ischemic symptoms; severe left ventricular malfunctioning; or a recent onset of arrhythmia, as well as when advanced diagnostic tests are needed (Gupta & Lipsitz, 2007; Moya et al., 2009). In addition, referral to a neurologist is indicated when advanced neurological diagnostic tests are required or with refractory autonomic failure (Gupta & Lipsitz, 2007). Furthermore, because nonpharmacological management is so important in OH care, patients may benefit from referral to a physical therapist for instruction on exercises and strategies to prevent OH symptoms (Feldstein & Weder, 2012; Figueroa et al., 2010; Gupta & Lipsitz, 2007).

Conclusion OH is a common syndrome seen with aging, often related to various diseases and medications (Fedorowski, Stavenow et al., 2010; Feldstein & Weder, 2012; Gupta & Lipsitz, 2007). Because this condition imposes a greater risk of individuals falling and becoming frail, and because it is related to high morbidity and mortality rates, it should be assessed thoroughly and managed well (Feldstein & Weder, 2012; Gupta & Lipsitz, 2007; Xue, 2011). Special consideration is needed for older people, as they may present with atypical symptoms because of comorbidity, and may be asymptomatic but still carry the risk of becoming symptomatic with acute changes in health (Figueroa et al., 2010; Gupta & Lipsitz, 2007). Therefore, it is reasonable for clinicians to screen for OH when encountering older people, as they have risks of OH, including their normal physiological changes, comorbidity, and polypharmacy, all of which can increase fall risk and tragic consequences (Chambers, 2005; Fedorowski, Stavenow et al., 2010; Raj, 2010). The pharmacological management of OH should only be considered after the failure of nonpharmacological attempts, and this should be accompanied with nonpharmacological man-

agement (Gupta & Lipsitz, 2007; Mansoor, 2006). The most commonly used medications are fludrocortisone, pyridostigmine, and midodrine (Figueroa et al., 2010; Gupta & Lipsitz, 2007). For OH management in the primary care setting, it is also necessary to be aware that many patients are diagnosed with OH when admitted to the hospital, as the admission status causes a longer bed stay, changes in medication and intake and output, and the administration of OH-inducing medication (Feldstein & Weder, 2012; Shibao et al., 2007). When transitioning from the hospital to the primary setting, careful evaluation of OH and whether or not to continue medications is needed (Feldstein & Weder, 2012). Lastly, many studies have stressed the necessity of revising and updating the consensus of the American Autonomic Society and the American Academy of Neurology in 1996, including the diagnostic criteria for OH and blood pressure measurement methods, with consideration of cumulative evidence-based studies since then (Fedorowski, Burri, & Melander, 2009; Wieling & Schatz, 2009).

References Abdel-Rahman, T. A. (2012). Orthostatic hypotension before and after meal intake in diabetic patients and healthy elderly people. Journal of Family and Community Medicine, 19(1), 20–25. doi:JFCM-19–20 [pii]10.4103/2230–8229.94007 Allan, L. M., Ballard, C. G., Rowan, E. N., & Kenny, R. A. (2009). Incidence and prediction of falls in dementia: A prospective study in older people. PLoS One, 4(5), e5521. doi:10.1371/journal.pone.0005521 Chambers, J. C. (2005). Should we screen hospice inpatients for orthostatic hypotension? Palliative Medicine, 19(4), 314–318. doi:10.1191/0269216305pm1027oa Coutaz, M., Iglesias, K., & Morisod, J. (2012). Is there a risk of orthostatic hypotension associated with antihypertensive therapy in geriatric inpatients? European Geriatric Medicine, 3(1), 1–4. doi:10.1016/j.eurger.2011.10.001 Fedorowski, A., Burri, P., & Melander, O. (2009). Orthostatic hypotension in genetically related hypertensive and normotensive individuals. Journal of Hypertension, 27(5), 976–982. ¨ Fedorowski, A., Engstrom, G., Hedblad, B., & Melander, O. (2010). Orthostatic hypotension predicts incidence of heart failure: The Malmo¨ preventive project. American Journal of Hypertension, 23(11), 1209–1215. doi:10.1038/ajh.2010.150 Fedorowski, A., Stavenow, L., Hedblad, B., Berglund, G., Nilsson, P. M., & Melander, O. (2010). Orthostatic hypotension predicts all-cause mortality and coronary events in middle-aged individuals (The Malmo Preventive Project). European Heart Journal, 31(1), 85–91. doi:ehp329 [pii]10.1093/eurheartj/ehp329 Feldstein, C., & Weder, A. B. (2012). Orthostatic hypotension: A common, serious and underrecognized problem in hospitalized patients. Journal of the American Society of Hypertension, 6(1), 27–39. doi:S1933–1711(11)00206–3 [pii]10.1016/j.jash.2011.08.008 Figueroa, J. J., Basford, J. R., & Low, P. A. (2010). Preventing and treating orthostatic hypotension: As easy as A, B, C. Cleveland Clinic Journal of Medicine, 77(5), 298–306. doi:77/5/298 [pii]10.3949/ccjm.77a.09118 Franke, W. D., Allbee, K. A., & Spencer, S.E. (2006). Cerebral blood flow responses to severe orthostatic stress in fit and unfit young and older adults. Gerontology, 52(5), 282–289. doi:10.1159/000094609

457

Orthostatic hypotension in older people

Gehrking, J. A., Hines, S. M., Benrud-Larson, L. M., Opher-Gehrking, T. L., & Low, P. A. (2005). What is the minimum duration of head-up tilt necessary to detect orthostatic hypotension? Clinical Autonomic Research, 15(2), 71–75. doi:10.1007/s10286–005–0246-y Gibbons, C. H., & Freeman, R. (2006). Delayed orthostatic hypotension: A frequent cause of orthostatic intolerance. Neurology, 67(1), 28–32. doi:67/1/28 [pii]10.1212/01.wnl.0000223828.28215.0b Gorelik, O., Almoznino-Sarafian, D., Litvinov, V., Alon, I., Shteinshnaider, M., Dotan, E., . . . Cohen, N. (2009). Seating-induced postural hypotension is common in older patients with decompensated heart failure and may be prevented by lower limb compression bandaging. Gerontology, 55(2), 138–144. doi:000141920 [pii]10.1159/000141920 Gray-Miceli, D., Ratcliffe, S. J., Liu, S., Wantland, D., & Johnson, J. (2012). Orthostatic hypotension in older nursing home residents who fall: Are they dizzy? Clinical Nursing Research, 21(1), 64–78. doi:10.1177/1054773811434045 Grubb, B. P. (2005). Neurocardiogenic syncope and related disorders of orthostatic intolerance. Circulation, 111(22), 2997–3006. doi:10.1161/CIRCULATIONAHA.104.482018 Gupta, V., & Lipsitz, L. A. (2007). Orthostatic hypotension in the elderly: Diagnosis and treatment. American Journal of Medicine, 120(10), 841–847. doi:S0002–9343(07)00363–4 [pii]10.1016/j.amjmed.2007.02.023 Jones, C. D., Loehr, L., Franceschini, N., Rosamond, W. D., Chang, P. P., Shahar, E., . . . Rose, K. M. (2012). Orthostatic hypotension as a risk factor for incident heart failure: The atherosclerosis risk in communities study. Hypertension, 59(5), 913–918. doi:HYPERTENSIONAHA.111.188151 [pii]10.1161/HYPERTENSIONAHA.111.188151 Kobayashi, K., & Yamada, S. (2011). Development of a simple index, calf mass index, for screening for orthostatic hypotension in community-dwelling elderly. Archives of Gerontology and Geriatrics, 54(2), 293–297. doi:S0167–4943(11)00087–2 [pii]10.1016/ j.archger.2011.04.003 Lamarre-Cliche, M., Souich, P., Champlain, J., & Larochelle, P. (2008). Pharmacokinetic and pharmacodynamic effects of midodrine on blood pressure, the autonomic nervous system, and plasma natriuretic peptides: A prospective, randomized, single-blind, two-period, crossover, placebo-controlled study. Clinical Therapeutics, 30(9), 1629–1638. doi:S0149–2918(08)00294–4 [pii]10.1016/j.clinthera.2008.09.001 Lee, T., Donegan, C., & Moore, A. (2005). Combined hypertension and orthostatic hypotension in older patients: A treatment dilemma for

458

Y. Lee

clinicians. Expert Review of Cardiovascular Therapy, 3(3), 433–440. doi:10.1586/14779072.3.3.433 Logan, I. C., & Witham, M. D. (2012). Efficacy of treatments for orthostatic hypotension: A systematic review. Age Ageing, 41(5), 587–594. doi:afs061 [pii]10.1093/ageing/afs061 Mansoor, G. A. (2006). Orthostatic hypotension due to autonomic disorders in the hypertension clinic. American Journal of Hypertension, 19(3), 319–326. doi:S0895–7061(05)01202–1 [pii]10.1016/j.amjhyper.2005.09.019 Medow, M. S., Stewart, J. M., Sanyal, S., Mumtaz, A., Sica, D., & Frishman, W. H. (2008). Pathophysiology, diagnosis, and treatment of orthostatic hypotension and vasovagal syncope. Cardiology in Review, 16(1), 4–20. doi:00045415–200801000–00002 [pii]10.1097 /CRD.0b013e31815c8032 Moya, A., Sutton, R., Ammirati, F., Blanc, J. J., Brignole, M., Dahm, J. B., . . . (HRS), Heart Rhythm Society. (2009). Guidelines for the diagnosis and management of syncope (version 2009). European Heart Journal, 30(21), 2631–2671. doi:ehp298 [pii]10.1093/eurheartj/ehp298 Poon, I. O., & Braun, U. (2005). High prevalence of orthostatic hypotension and its correlation with potentially causative medications among elderly veterans. Journal of Clinical Pharmacology and Therapeutics, 30(2), 173–178. doi:JCP629 [pii]10.1111/j.1365–2710.2005.00629.x Raj, S. R. (2010). Highlights in clinical autonomic neurosciences: Orthostatic tachycardia and orthostatic hypotension. Autonomic Neuroscience, 154(1–2), 1–2. doi:S1566–0702(10)00043–3 [pii]10.1016/j.autneu.2010.02.004 Shibao, C., Grijalva, C. G., Raj, S. R., Biaggioni, I., & Griffin, M. R. (2007). Orthostatic hypotension-related hospitalizations in the United States. American Journal of Medicine, 120(11), 975–980. doi:S0002–9343(07)00655–9 [pii]10.1016/j.amjmed.2007.05.009 Vetta, F., Ronzoni, S., Costarella, M., Donadio, C., Battista, L., Renzulli, G., . . . Zuccaro, S. M. (2009). Recurrent syncope in elderly patients and tilt test table outcome: The role of comorbidities. Archives of Gerontology and Geriatrics, 49(Suppl 1), 231–236. doi:S0167–4943(09)00234–9 [pii]10.1016/j.archger.2009.09.034 Wieling, W., & Schatz, I. J. (2009). The consensus statement on the definition of orthostatic hypotension: A revisit after 13 years. Journal of Hypertension, 27(5), 935–938. doi:00004872–200905000–00004 [pii]10.1097/HJH.0b013e32832b1145 Xue, Q. L. (2011). The frailty syndrome: Definition and natural history. Clinics in Geriatric Medicine, 27(1), 1–15. doi:S0749–0690(10)00083–2 [pii]10.1016/j.cger.2010.08.009