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http://orcid.org/0000-0002-4605-5344
Abstract
Abstract
Purpose: Orthostatic hypotension (OH) is a common and clinically important disorder. Published papers vary regarding the definitions of OH and methodologies of evaluation. Moreover, substantial gaps in the skills and knowledge required for assessment of OH have been reported by clinicians. We aimed to provide current information regarding the definition, classification and evaluation of OH.
Methods: We performed a comprehensive search of medical databases, using the following keywords: “postural hypotension” or “orthostatic hypotension”, combined with: “definition”, “classification”, “diagnosis”, “evaluation” or “meaning”. We selected for this review the most relevant recent publications and key papers in the field, published in the English language.
Results: Current data regarding definitions, classification and the evaluation of OH are reviewed. The various aspects of OH assessment are extensively discussed. Considerable discrepancies exist between the published guidelines regarding the methodology of OH diagnosing. We propose an algorithm for OH evaluation and a standardized protocol for bedside determination of OH by healthcare providers.
Conclusions: Correct assessment of OH is essential for its accurate diagnosis. The methodology of OH evaluation has not been sufficiently standardized. We emphasize the clinical importance of the uniform investigation of OH, according to the current guidelines for OH definition and meaning.
Introduction
Orthostatic hypotension (OH) is a common and frequently unrecognized disorder [1–3]. OH is strongly associated with increased risks of recurrent falls [1–5], cardiovascular disorders [1–3,6–8] and death [1–3,6–9].
Substantial discrepancies have been reported between published studies regarding the OH definition and its meaning [10,11]. The methodology of OH evaluation has not been sufficiently standardized [10–12]. Moreover, considerable gaps in the skills and knowledge required for the assessment of OH have been observed among healthcare providers [13,14].
We aimed to provide current information regarding the definition, classification and evaluation of OH, and to emphasize the clinical importance of standardization in OH assessment.
Methods
A comprehensive search of PubMed, Embase and Google Scholar databases was performed for potentially relevant articles published in the English language until March 2019, using the following keywords: “postural hypotension” or “orthostatic hypotension”, combined with “definition”, “classification”, “diagnosis”, “evaluation” or “meaning”. Reference lists of all eligible papers were also searched for additional relevant studies. This review was based on the most important recent publications and key papers in the field.
OH definition
OH, also called postural hypotension, has been traditionally defined as a fall of at least 20 mmHg in systolic blood pressure (BP) and/or of at least 10 mmHg in diastolic BP within 3 min of active standing or head-up tilt table testing (HUTT) at an angle of at least 60˚ [15,16]. In addition to classic OH (within 30 sec–3 min of standing) [15,16], two other variants of OH have been described: initial (within 15 sec of standing) [17] and delayed (after more than 3 min of standing) [18]. In 2009, Fedorowski et al. suggested that the above-mentioned criteria for diagnosis of OH should be modified in patients with high or low supine BP [19,20]. Thus, in patients with supine hypertension (BP ≥160 mmHg), an orthostatic fall in systolic BP of at least 30 mmHg was recommended to define OH, because the magnitude of the BP drop depends on the baseline BP [19]. Moreover, for patients with supine systolic BP less than 120 mmHg, a postural decline in systolic BP of 15 mmHg or under 90 mmHg may indicate OH, since these individuals are more likely to be symptomatic [19].
In 2011, the definition of OH was updated and endorsed by the American Autonomic Society, the European Federation of Autonomic Societies, the Autonomic Research Group of the World Federation of Neurology and the Autonomic Disorders section of the American Academy of Neurology [21]. According to this consensus statement, the traditional definition of OH is recommended for normotensive persons [21]. However, in hypertensive patients, a reduction in systolic BP of 30 mmHg is required to define OH [21]. Recently published guidelines of the European Society of Cardiology propose an additional criterion for OH definition: a systolic BP drop to <90 mmHg, irrespective of the magnitude of the BP fall [12].
OH classification
Table 1 presents the classification of OH. According to a period of OH occurrence during orthostatic stress, three forms of OH are currently recognized: classic, initial and delayed [1–3,21,22].
Table 1. Classification of OH.
Classic OH
Classic OH is the most common and typical variant of orthostatic intolerance. It is defined as a sustained decline in systolic and/or diastolic BP (according to the current criteria for OH) within 30 to 180 sec of active standing or HUTT [1–3,21,22]. Classic OH is caused by decreased total peripheral resistance and/or an excessive fall of cardiac output, such that compensatory vasoconstrictor mechanisms are not sufficient to restore postural BP decline [1–3,21,22].
Initial OH
In contrast to the classic and delayed forms, initial OH is defined as a transient drop of >40 mmHg in systolic BP and/or >20 mmHg in diastolic BP within 15 sec of active standing [1–3,16,21,22]. The proposed underlying pathophysiologic mechanism is a temporal and abrupt mismatch between cardiac output and total peripheral resistance [16]. Initial OH is frequently symptomatic and a common cause of situational syncope, which may be underrecognized [16].
Delayed OH
Delayed OH is defined as a sustained fall in BP (according to the current criteria for classic OH) occurring after 3–45 min of active standing or HUTT [1–3,17,21,22]. The possible pathophysiologic mechanisms of delayed OH include increased pooling in the lower body capacitance vessels and gradual impairment of compensatory mechanisms during prolonged orthostatic stress, resulting in slow progressive declines in venous return to the heart, cardiac output and BP [3,17,22]. Delayed OH is considered a mild form of classic OH and may progress to classic OH [3,17,22].
Systolic and diastolic OH
Modalities of OH included isolated systolic, isolated diastolic and combined (systolic and diastolic) OH. Systolic OH is currently defined as a drop in systolic BP during orthostatic stress of ≥20 mmHg or <90 mmHg in normotensive patients, or of ≥30 mmHg in patients with supine hypertension [12,21]. The current definition of diastolic OH is a postural fall of ≥10 mmHg in diastolic BP [12,21]. Systolic OH has received more attention in the medical literature than diastolic OH. Thus, some studies have investigated only systolic OH [23–26]. Information regarding differences between systolic and diastolic OH is limited. In several studies of community-dwelling persons, systolic vs. diastolic OH prevailed [27,28]. In a number of studies of hospitalized patients, the rates of systolic and diastolic OH were comparable [29,30]. However, diastolic OH was more frequently observed than systolic OH among patients in acute geriatric wards [31]. Differences in the study populations and design may explain these discrepancies. Systolic OH is more likely to be symptomatic [28,32] and indicates higher risk of stroke [33] than does diastolic OH. However, diastolic OH more strongly predicts myocardial infarction [6,33,34] and mortality [35] than systolic OH.
Etiologic OH classification
According to the etiology, OH is classified as having a primary or secondary origin (Table 1) [2,36]. Primary OH is rare and caused by chronic autonomic failure, resulting from Parkinson's disease, multiple system atrophy, pure autonomic failure and other primary neurodegenerative disorders [2,36]. Secondary OH is common and occurs as a consequence of a variety of predisposing conditions such as: the use of certain drugs, hypovolemia, venous pooling, cardiovascular disorders, diabetes mellitus, renal failure, autoimmune diseases and endocrinopathies [2,36].
Pathophysiologic OH classification
According to the major underlying mechanism, OH is divided into neurogenic (structural) and non-neurogenic (functional) categories (Table 1) [1–3]. Neurogenic OH may be primary (due to the above-mentioned primary neurodegenerative disorders) or secondary (related to polyneuropathies) [1–3,36]. Table 2 details causes of neurogenic OH. The main pathophysiologic mechanism for the development of neurogenic OH is a severe decrease in total peripheral resistance, resulting from chronic progressive failure of the autonomic nervous system [1–3]. Non-neurogenic OH is caused by an excessive fall in cardiac output, such that intact compensatory mechanisms are not sufficient to restore BP decline, or by a less severe decrease in cardiac output accompanying a mild or transient impairment of vasoconstrictor compensatory mechanisms [1–3]. Non-neurogenic OH is more common than neurogenic, and is associated with aging, hypovolemia, venous pooling, comorbidities and certain medications (Table 3) [1–3,6,11,37].
Table 2. Causes of neurogenic OH.
Table 3. Causes of non-neurogenic OH.
OH classification according to clinical course
The presentation of OH may be acute or chronic [2,11,38]. Acute OH occurs more often than chronic and is caused by temporary non-neurogenic factors such as: blood loss, dehydration, treatment with certain drugs and immobility [11,38]. Recognizing acute OH is important because it is frequently symptomatic and potentially reversible after correction of the underlying cause (blood and fluid replacement, withdrawal of offending medication and ambulation) [11,37,38]. Chronic OH may present as a progressive disabling illness (neurogenic OH) or as a less severe disorder that is related to non-neurogenic predisposing and contributing conditions (older age, cardiovascular disorders and renal failure) [2,3].
OH classification according to the presence of symptoms
OH may be asymptomatic or symptomatic [1–3,21,22]. Symptoms of OH include dizziness, light-headedness, visual blurring, palpitations, fatigue, “coat-hanger” pain (neck pain and headache localized in the suboccipital, posterior cervical and shoulder region), angina pectoris and syncope [1–3,21]. The association of symptoms with OH is not consistent [2,10,11,22]. Thus, most community-dwelling patients with OH are asymptomatic [1,2,39,40]. However, typical OH symptoms are very common among elderly hospitalized patients, while a measurable OH may not be detected [11,37]. A weak correlation of patient's complaints with OH may be explained by the low specificity of symptoms with an orthostatic BP decline [2,10,11]. In addition, the threshold for the appearance of OH symptoms is determined by the complexity of individual cerebral hemodynamic regulation, and depends more on the absolute BP level than the magnitude of the fall [2,10,11,22,40,41]. Thus, it has been suggested that OH may be alternatively defined as any, rather than an arbitrarily stated, orthostatic BP drop, which results in symptoms that refer to cerebral hypoperfusion [10,41].
Ricci et al. have classified OH into four functional classes, according to the severity and frequency of symptoms (Table 1) [2]. In functional class I, patients are usually asymptomatic and only occasionally demonstrate OH symptoms. In patients with class II, the symptoms occur weekly or monthly, and result in mild to moderate limitation of daily living activities. Functional class III is characterized by more severe and frequent symptoms, with marked limitation in daily living activities. In functional class IV, severe symptoms persist on a daily basis, leading to disability.
OH evaluation
Indications for OH evaluation
Indications for the assessment of OH include a history or presence of: a typical OH manifestation (fall, syncope, dizziness, lightheadedness, visual disturbance or palpitation); or, in asymptomatic patients, a condition in which OH frequently occurs (older age, neurodegenerative disease, hypertension, heart failure, diabetes mellitus, renal failure, amyloidosis, autoimmune disorder or treatment with offending medications) [1,2].
History taking
A thorough anamnesis should be taken with a detailed description of symptoms and determination of predisposing factors for OH [1,16,42].
The occurrence of typical symptoms such as dizziness or loss of consciousness during standing only, immediately after exercise or following meals, or during exposure to a hot environment, is highly suggestive of OH [3,12,42]. In initial OH, orthostatic symptoms typically appear immediately after standing-up, following prolonged bed rest or after arising from the squatting position, and disappear within 20–30 sec [17]. Delayed OH is characterized by prolonged prodromes with typical orthostatic complaints that may be followed by reflex syncope [18]. Classically, symptoms of OH should be relieved by seating or lying down [42].
A careful history should be taken regarding possible contributors to OH: environmental factors, dehydration, bleeding, bed rest and chronic comorbidities [1,16,42]. In addition, detailed information should be obtained regarding the use of medications that can cause or aggravate OH (Table 3) [1,16,42].
Clinical evaluation
The performance of a detailed physical examination, 12-lead electrocardiogram recording and routine laboratory tests are recommended for initial assessment of OH [1,2,16]. This evaluation may be helpful to identify the cause or aggravating factors for OH. Further investigations depend on the possible underlying disorder [2,16].
Methods for OH evaluation
Currently, three methods are recommended for determination of OH: bedside orthostatic test, HUTT and ambulatory BP monitoring (ABPM) [1,2,12,42]. In addition, home BP monitoring (HBPM) may be considered to detect OH [12,43,44].
The bedside orthostatic test
The bedside orthostatic test is the method of choice for diagnosing OH [2,10]. It is easy to perform, available and inexpensive. This test may be performed in three ways: lying-to-standing, sitting-to-standing and lying-to-sitting [10].
Active standing-up from the supine position is the “gold standard” method for initial evaluation of OH [2,12,16]. However, for patients with difficulty or inability to stand, OH may be assessed during passive transition from lying to the sitting position only [37,45]. Moreover, the evaluation of seated OH is recommended in patients at a high risk for symptomatic standing OH, such as elderly hospitalized patients during ambulation after acute illness [11,37,45].
OH evaluation on transition from the sitting to the standing position has been reported in some studies [26,46,47]. This method entails shorter time than the other bedside orthostatic tests, and is considered a screening test in patients with hypertension [43] or as an alternative to the supine-standing assessment in a busy practice [42,46]. Moreover, standing-up from a squatting position has been recommended for determination of initial OH [17]. However, sit-to-stand testing has lower diagnostic accuracy in detecting OH than the standard orthostatic tests [10,42,46].
HUTT
HUTT is an alternative method for diagnosing OH [2,10,12]. It is not always available, requires special laboratory equipment and depends on interpretation by an expert [2]. The use of HUTT is generally reserved for assessment of OH in patients with a negative bedside orthostatic test whose complaints are strongly suggestive of OH [2,12,16,37]. However, HUTT is less sensitive than active standing-up for confirmation of initial OH [2,3,17]. The methodology of HUTT is not standardized [10,12]. Protocols for performing HUTT vary in the durations of the supine pre-tilt and the passive head-up tilt, the tilt angle and the monitoring of hemodynamic parameters [10,12].
ABPM
Twenty-four-hour ABPM is a widely used technique for confirming hypertension and evaluating BP control [43,48]. BP measurements should be obtained every 15–30 minutes during a 24-hour period, and at least 70% of expected measurements must be recorded (at least 20 awake and 7 asleep valid BP determinations) [48,49].
ABPM is considered a helpful method for OH evaluation [2,12,43,48,49]. Diagnosis of OH by ABPM is based on diurnal variation of systolic and diastolic BP. Reduced dipping (night/day fall ≤10% in mean values of BP) and reverse dipping (night/day increase in average BP levels) are patterns of diurnal BP variation that associate strongly with OH [49–52]. ABPM may be helpful for diagnosing masked OH (OH that is not detected in the office) and postprandial OH [12,48,49,53]. In addition, ABPM is recommended for patients with established OH, for assessment of nocturnal hypertension, drug-induced OH and OH severity, and also for tailoring treatment and diagnosing of additional comorbidities such as obstructive sleep apnea, nocturnal movement disorders and sleep dysfunction [2,12,48,49,53]. We suggest that ABPM may be repeated at intervals of 3–6 months or even more frequently, as in certain situations such as reassessment of acute OH or following change in treatment of chronic OH.
HBPM
HBPM is one of the methods recommended for diagnosing and treating hypertension [43,54]. This technique consists of repeated BP measurements performed outside the clinical setting [43,54]. A standardized protocol of BP measurement for HBPM has not been established [44,54]. The most common recommendation is determination of BP in a sitting position, twice in the morning and twice in the evening, with 1-minute intervals for 7 consecutive days [54]. However, isolated BP measurements on two occasions and 3-day duration of the evaluation have also been reported as a sufficient approach for correct BP assessment [54].
HBPM has recently been reported as an easily feasible, simple and inexpensive method for assessment of OH [43,44]. HBPM can identify masked OH, assess day-to-day OH variability and contribute to the determination of optimal treatment of OH [12,43,44]. Information about evaluating OH by HBPM is limited. In one study, the following protocol was reported: three consecutive BP determinations in a sitting position and a single BP measurement following standing, performed twice daily (in the morning after waking up and in the evening after dinner) [44]. This assessment was repeated over 3 consecutive days. Among 505 patients, the use of HBPM increased OH reproducibility compared to assessment in a clinical setting (the respective rates of detected OH were 37% and 15%) [44]. Thus, this HBPM protocol seems accurate for OH screening. We suggest that in additional situations, such as differentiation of acute from chronic OH or tailoring treatment of chronic OH, OH may be evaluated by HBPM over a longer period, at 1-week or 1-month intervals. Future longitudinal studies should be conducted to delineate, substantiate and broaden our knowledge about the optimal role of HBPM in the evaluation and management of OH.
Considering the available data regarding the methods for OH evaluation, current guidelines do not sufficiently detail and standardize the determination of OH. We propose a user-friendly algorithm for diagnosing OH, which summarizes the available methods for OH evaluation and generally follows the recent guidelines (Figure 1).
Published online:
15 April 2019Figure 1. Proposed algorithm for the diagnosis of OH. OH: orthostatic hypotension; BOT: bedside orthostatic test; HUTT: head-up tilt table testing; ABPM: ambulatory blood pressure monitoring; HBPM: home blood pressure monitoring.
![]({"type":"image","src":"/na101/home/literatum/publisher/tandf/journals/content/iblo20/2019/iblo20.v028.i03/08037051.2019.1604067/20200214/images/medium/iblo_a_1604067_f0001_b.jpg"})
Figure 1. Proposed algorithm for the diagnosis of OH. OH: orthostatic hypotension; BOT: bedside orthostatic test; HUTT: head-up tilt table testing; ABPM: ambulatory blood pressure monitoring; HBPM: home blood pressure monitoring.
Duration of bed rest prior to orthostatic stress
In assessment of OH, there is no consensus regarding the optimal time for supine rest before a change of posture [10,11,37,55,56]. In clinical studies, the reported supine resting time varied from 5 min to 7 days [10,11,55,56]. Bed rest duration of 5 min before starting a postural challenge is considered an acceptable minimum [10,11,37,42,43]. However, limiting lying time to 5 min may miss the substantial number of OH cases that may be diagnosed after bed rest lasting longer than 5 min [55,56].
Bed rest is a well-known risk factor for OH, especially in elderly hospitalized patients [11,20,7,38,57]. Supine rest increases blood pooling in low body capacitance vessels and enhances diuresis due to suppressed release of antidiuretic hormone; this results in aggravation of the orthostatic decline in the venous return to the heart and cardiac output [11,20,37,38,57]. Moreover, immobility impairs a compensatory response to orthostatic stress via attenuation of baroreceptor function [36,57]. No large high-quality studies have been conducted on the relationship of supine rest duration and OH. In a study of 121 older inpatients, the respective rates of OH on the first morning standing-up were significantly higher in those with bed rest lasting >8 hours than in those with bed rest ≤8 hours (71.3% vs. 30.0%, p < 0.001) [30]. In another study, of 108 older patients hospitalized for acutely decompensated heart failure, each 1-hour increment of bed rest strongly predicted the occurrence of seated OH (relative risk 1.58 and 95% confidence interval 1.13–2.20) [58].
Summarizing the data, a minimal supine time of 5 min before starting BP measurements is recommended for routine OH evaluation. However, in patients with typical OH symptoms and a negative initial orthostatic test, OH may be reassessed after a period of bed rest extending up to 10–20 min.
Technique of measuring BP in the assessment of OH
BP may be measured by a variety of devices. Noninvasive continuous beat-to-beat finger BP monitoring may detect rapid and transient hemodynamic changes during standing, and this is the only technique available for diagnosing initial OH [12,17,59–61]. However, OH determination using noninvasive continuous BP monitoring is usually limited to research and tilt laboratories [10,60]. In general practice, BP is routinely measured intermittently by auscultatory or oscillometric devices that may be manual, semiautomatic or automatic [10,43,62]. The devices should be regularly validated according to standardized protocols [10,43,62].
Accuracy and standardization in BP measurement are important for correct diagnosis of OH. Vloet et al. evaluated the skills and knowledge of 170 nurses in measuring BP for OH determination [13]. Substantial differences in the assessment of OH were observed between the nurses. The most important and frequent deviations from the published guidelines, leading to inaccurately diagnosing OH, were: incorrect placement of the cuff during the BP measurements and varied time for standing BP determinations (range 0–30 min) [13]. O'Riordan et al. recently evaluated a technique of BP measurement in the assessment of OH among 275 physicians, nurses and physiotherapists; the recording BP and the interpretation of the findings varied greatly between healthcare providers [14].
Ideally, orthostatic testing should be undertaken in a quiet room, at a temperature 20–24 °C, after comfortable bed rest and with an empty bladder [16,62]. The patient should avoid caffeine, exercise and smoking for at least 30 min before the assessment [62]. All clothing covering the location of cuff placement should be removed [62]. The current guidelines recommend using an upper arm cuff with appropriate size: a standard cuff, of 12–13 cm width and 35 cm length for most patients, but longer (40 cm length) for persons with obesity and shorter (18 cm length) for lean individuals [43,62]. The middle of the cuff should be placed on the brachial artery at the level of the right atrium (the midpoint of the sternum), with the arm supported, to avoid increasing BP by muscle contraction and isometric exercise [42,62]. The first BP measurements should be performed on both arms to detect possible differences between the arms, and the arm with the higher BP value should be considered the reference [43,62]. According to current guidelines of the European Society of Hypertension and the European Society of Cardiology, three BP measurements should be recorded, 1–2 min apart, and additional measurements should be performed only if the first two readings differ by >10 mmHg; thus, the average of the two last readings is recorded as the baseline BP [43].
During an orthostatic test, BP and heart rate should be assessed [10,16,42,43]. In addition, the patient should be asked to report the appearance of OH symptoms [10]. For safety reasons, measures should be taken to prevent falls, and in patients with severe OH symptoms or low BP, the test should be aborted with immediate return to the lying position [36,58].
The optimal duration of the orthostatic stress is not clear. The period of 3 min after change of posture is generally accepted [15,16,20,21,42,43], though insufficient for detecting delayed OH [18]. Thus, in patients suspected of having delayed OH, an extended evaluation of OH (to at least 20 min) has been recommended [18]. Other authors have proposed a shorter duration (within 5 min of standing) for assessment of delayed OH [1,2,10]. We suggest that the determination of OH at intervals of 1 − 3 − 5 − 10 min after change of posture may a provide balance between the possible misdiagnosis of delayed OH and the time consumed in a busy practice [11,57].
Summarizing the published data, substantial variations exist in the techniques available for performing the orthostatic test. We call for standardization and recommend using a simple structured protocol for bedside assessment of OH (Figure 2).
Published online:
15 April 2019Figure 2. Recommended standardized protocol for bedside assessment of OH. OH: orthostatic hypotension; BP: blood pressure.
![]({"type":"image","src":"/na101/home/literatum/publisher/tandf/journals/content/iblo20/2019/iblo20.v028.i03/08037051.2019.1604067/20200214/images/medium/iblo_a_1604067_f0002_b.jpg"})
Figure 2. Recommended standardized protocol for bedside assessment of OH. OH: orthostatic hypotension; BP: blood pressure.
Validity of OH testing
Inconsistent reproducibility and high variability in OH have been reported [10,36]. Variability in the diurnal, day-to-day and seasonal patterns of OH is well recognized [10,21,37]. Sources of OH variability include effects of environmental factors, meals, medications and volume depletion, as well as differences in OH determination such as: supine rest duration, accuracy of BP measurement, length of time for standing BP assessment and the number of orthostatic tests [10,11,37].
The occurrence of OH during a single orthostatic test is sufficient for diagnosis, while a negative test on one occasion does not exclude OH [10,42]. For patients with possible OH and not demonstrating OH on the first determination, OH should be reevaluated at different times on other days [10,42]. Preferably, OH should be reassessed at the time of the day when symptoms occur or after a possibly predisposing situation such as meals, exercise, morning standing-up and taking of medications [42]. In addition, the repeated assessment of OH over time may help to differentiate acute from chronic OH [10].
Management of OH
Current management of OH is based on non-pharmacologic and pharmacologic measures [2,3,12]. First steps to avoid OH and to prevent falls involve non-pharmacologic interventions. Patients should be educated regarding the possible avoidance of precipitating factors such as: prolonged standing, large meals, over-heating and offending medications, and also regarding the early recognition of prodromal OH symptoms in order to change position to sitting or lying [2,3,12]. Additional non-pharmacologic measures include: increased salt and water intake, slow rising, raising the head of the bed during sleeping, leg crossing while standing, and the use of compression garments on the abdomen or lower extremities [2,3,12]. Pharmacologic treatment (midodrine, fludrocortisone, pyridostigmine, droxidopa and other medications) is recommended for patients who demonstrate chronic symptomatic OH despite non-pharmacologic interventions [2,3,12]. Management of OH has been addressed extensively in a number of excellent recent papers [2,3,12] and is beyond the scope of this review.
Conclusion
In the present state-of-the-art review, we provided current information regarding definitions, classification and evaluation of OH. The various aspects of methodology for OH assessment were extensively discussed. Substantial discrepancies were found between the published guidelines regarding protocols for OH determination. We emphasize the importance of correct assessment for accurate diagnosis of OH, and call for better standardization of OH evaluation. We also proposed a detailed algorithm for diagnosing OH and a structured protocol for bedside assessment of OH; these generally follow the current guidelines for OH investigation.
| Classification of OH | Comments |
|---|---|
| According to a period of occurrence during orthostatic stress | |
| Initial OH | Occurred within 15 sec |
| Classic OH | Occurred within 30 to 180 sec |
| Delayed OH | Occurred after 3–45 min |
| According to the relationship of OH to different parts of the cardiac cycle | |
| Isolated systolic OH | Drop in systolic BP of ≥20 or <90 mmHg in normotensive patients, or of ≥30 mmHg in patients with supine hypertension |
| Isolated diastolic OH | Fall in diastolic BP of ≥10 mmHg |
| Combined OH | Systolic and diastolic OH |
| According to the etiology | |
| Primary OH | Caused by primary neurodegenerative disorders |
| Secondary OH | Caused by conditions resulting in secondary autonomic failure |
| According to the pathophysiology | |
| Neurogenic (structural) OH | Related to chronic progressive failure of the autonomic nervous system |
| Non-neurogenic (functional) OH | Related to an excessive fall in cardiac output or a less severe decrease in cardiac output accompanying a mild or transient autonomic failure |
| According to the clinical course | |
| Acute OH | Caused by temporary factors (hypovolemia, venous pooling and medications) |
| Chronic OH | Related to neurogenic OH or chronic non-neurogenic conditions (older age, cardiovascular disorders and renal failure) |
| According to the presence of symptoms | |
| Asymptomatic OH | Common |
| Symptomatic OH | Symptoms include dizziness, light-headedness, visual blurring, palpitations, fatigue, "coat-hanger" pain, angina pectoris and syncope |
| According to the clinical severity | |
| Functional class I | Patients only occasionally demonstrate OH symptoms |
| Functional class II | Symptoms occur weekly or monthly and result in mild to moderate limitations in daily living activities |
| Functional class III | Symptoms are more severe and frequent, with marked limitation in daily living activities |
| Functional class IV | Persistence of severe symptoms on a daily basis, leading to disability |
| According to the means of testing | |
| Standing OH | May be diagnosed on lying-to-standing (the "gold standard" method for initial evaluation of OH) or on sitting-to-standing (the alternative method for OH assessment in a busy practice) |
| Seated OH | For patients unable to stand or at a high risk for symptomatic standing OH, OH may be evaluated on the lying-to-sitting test |
OH: orthostatic hypotension; BP: blood pressure.
| Primary neurodegenerative disorders |
| Parkinson's disease |
| Dementia with Lewy body |
| Multiple system atrophy |
| Pure autonomic failure |
| Autoimmune autonomic gangliopathy |
| Familial dysautonomia |
| Dopamine beta-hydrolase deficiency |
| Idiopathic |
| Secondary polyneuropathies |
| Endocrine disorders (diabetes mellitus, adrenal insufficiency and hypothyroidism) |
| Malignant diseases (amyloidosis, multiple myeloma and paraneoplastic syndromes) |
| Autoimmune diseases (lupus, Sjogren's syndrome, rheumatoid arthritis, celiac disease, Guillain- |
| Barré syndrome and multiple sclerosis) |
| Exposure to toxins (alcoholism, chemotherapy and poisoning by industrial chemicals) |
| Nutritional deficiencies (vitamins B1, B6, B12 and E) |
| Infections (herpes zoster, human immunodeficiency virus, Lyme disease, hepatitis B and C) |
| Posttraumatic |
| Uremia |
| Liver cirrhosis |
| Hereditary disorders |
OH: orthostatic hypotension.
| Aging |
|---|
| Volume depletion |
| Blood loss |
| Dehydration |
| Venous pooling |
| Prolonged immobility |
| Deconditioning |
| Postprandial |
| Exposure to hot and humid environment |
| Extensive varicose veins |
| Cardiovascular disorders |
| Hypertension |
| Heart failure |
| Cardiac arrhythmias |
| Aortic stenosis |
| Hypertrophic obstructive cardiomyopathy |
| Renal failure |
| Medications |
| Diuretics |
| Vasodilators (alpha-receptor blockers, calcium channel blockers, hydralazine, nitrates, angiotensin-converting |
| enzyme inhibitors and angiotensin receptor blockers) |
| Central sympatholytics |
| Beta-receptor blockers |
| Psychotropic agents (antidepressants, tranquilizers and antipsychotics) |
| Anti-Parkinsonian agents |
OH: orthostatic hypotension.
Disclosure statement
The authors report no conflict of interest.
References
- Fedorowski A, Melander O. Syndromes of orthostatic intolerance: a hidden danger. J Intern Med. 2013;273:322–335. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Ricci F, De Caterina R, Fedorowski A. Orthostatic hypotension: epidemiology, prognosis, and treatment. J Am Coll Cardiol. 2015;66:848–860. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Freeman R, Abuzinadah AR, Gibbons C, et al. Orthostatic hypotension: JACC state-of-the-art review. J Am Coll Cardiol. 2018;72:1294–1309. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Finucane C, O'Connell MD, Donoghue O, et al. Impaired orthostatic blood pressure recovery is associated with unexplained and injurious falls. J Am Geriatr Soc. 2017;65:474–482. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Mol A, Bui Hoang PTS, Sharmin S, et al. Orthostatic hypotension and falls in older adults: a systematic review and meta-analysis. J Am Med Dir Assoc. 2018. doi:10.2016/j.jamda.2018.11.003 [Epub ahead of print]. [Crossref], [PubMed], [Google Scholar]
- Fedorowski A, Stavenow L, Hedblad B, et al. Orthostatic hypotension predicts all-cause mortality and coronary events in middle-aged individuals (The Malmö Preventive Project). Eur Heart J. 2010;31:85–91. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- 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;36:1609–1617. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Chou RH, Liu CJ, Chao TF, et al. Association between orthostatic hypotension, mortality, and cardiovascular disease in Asians. Int J Cardiol. 2015;195:40–44. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- 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;114:630–636. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Naschitz JE, Rosner I. Orthostatic hypotension: framework of the syndrome. Postgrad Med J. 2007;83:568–574. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Tzur I, Izhakian S, Gorelik O. Orthostatic hypotension in internal medicine wards. Curr Med Res Opin. 2018. doi:10.1080/03007995.2018.1546679 (Epub ahead of print). [Taylor & Francis Online], [Web of Science ®], [Google Scholar]
- Brignole M, Moya A, de Lange FJ, et al. ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39:1883–1948. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Vloet LC, Smits R, Frederiks CM, et al. Evaluation of skills and knowledge on orthostatic blood pressure measurements in elderly patients. Age Ageing. 2002;31:211–216. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- O'Riordan S, Vasilakis N, Hussain L, et al. Measurement of lying and standing blood pressure in hospital. Nurs Older People. 2017;29:20–26. [Crossref], [PubMed], [Google Scholar]
- 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. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Lahrmann H, Cortelli P, Hilz M, et al. EFNS guidelines on the diagnosis and management of orthostatic hypotension. Eur J Neurol. 2006;13:930–936. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Wieling W, Krediet CT, van Dijk N, et al. Initial orthostatic hypotension: review of a forgotten condition. Clin Sci. 2007;112:157–165. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Gibbons CH, Freeman R. Delayed orthostatic hypotension: a frequent cause of orthostatic intolerance. Neurology 2006;67:28–32. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Fedorowski A, Burri P, Melander O. Orthostatic hypotension in genetically related hypertensive and normotensive individuals. J Hypertens. 2009;27:976–982. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Wieling W, Schatz IJ. The consensus statement on the definition of orthostatic hypotension: a revisit after 13 years. J Hypertens. 2009;27:935–938. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- 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;21:69–72. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Brignole M, Moya A, de Lange FJ, et al. Practical Instructions for the 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39:e43–e80. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Harris T, Lipsitz LA, Kleinman JC, et al. Postural change in blood pressure associated with age and systolic blood pressure. The National Health and Nutrition Examination Survey II. J Gerontol. 1991;46:M159–M163. [Crossref], [PubMed], [Google Scholar]
- Räihä I, Luutonen S, Piha J, et al. Prevalence, predisposing factors, and prognostic importance of postural hypotension. Arch Intern Med. 1995;155:930–935. [Crossref], [PubMed], [Google Scholar]
- Puisieux F, Boumbar Y, Bulckaen H, et al. Intraindividual variability in orthostatic blood pressure changes among older adults: the influence of meals. J Am Geriatr Soc. 1999;47:1332–1336. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Townsend RR, Chang TI, Cohen DL, et al. Orthostatic changes in systolic blood pressure among SPRINT perticipants at baseline. J Am Soc Hypertens. 2016;10:847–856. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Luukinen H, Koski K, Laippala P, et al. Prognosis of diastolic and systolic orthostatic hypotension in older persons. Arch Intern Med. 1999;159:273–280. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Fedorowski A, Hamrefors V, Sutton R, et al. Do we need to evaluate diastolic blood pressure in patients with suspected orthostatic hypotension? Clin Auton Res. 2017;27:167–173. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Cohen N, Gorelik O, Fishlev G, et al. Seated postural hypotension is common among older inpatients. Clin Auton Res. 2003;13:447–449. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Gorelik O, Fishlev G, Litvinov V, et al. First morning standing up may be risky in acutely ill older inpatients. Blood Press. 2005;14:139–143. [Taylor & Francis Online], [Web of Science ®], [Google Scholar]
- Weiss A, Grossman E, Beloosesky Y, et al. Orthostatic hypotension in acute geriatric ward: is it a consistent finding? Arch Intern Med. 2002;162:2369–2374. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Romero-Ortuno R, Cogan L, Fan CW, et al. Intolerance to initial orthostasis relates to systolic BP changes in elders. Clin Auton Res. 2010;20:39–45. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Fedorowski A, Wahlstrand B, Hedner T, et al. Systolic and diastolic component of orthostatic hypotension and cardiovascular events in hypertensive patients: the Captopril Prevention Project. J Hypertens 2014;32:75–81. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Luukinen H, Koski K, Laippala P, et al. Orthostatic hypotension and the risk of myocardial infarction in the home-dwelling elderly. J Intern Med. 2004;255:486–493. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Lagro J, Laurenssen NC, Schalk BW, et al. Diastolic blood pressure drop after standing as a clinical sign for increased mortality in older falls clinic patients. J Hypertens. 2012;30:1195–1202. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Goldstein DS, Robertson D, Esler M, et al. Dysautonomias: clinical disorders of the autonomic nervous system. Ann Intern Med. 2002;137:753–763. [Crossref], [PubMed], [Google Scholar]
- Feldstein C, Weder AB. Orthostatic hypotension: a common, serious and underrecognized problem in hospitalized patients. J Am Soc Hypertens. 2012;6:27–39. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Memmer MK. Acute orthostatic hypotension. Heart Lung. 1988;17:134–143. [PubMed], [Web of Science ®], [Google Scholar]
- Rutan GH, Hermanson B, Bild DE, et al. Orthostatic hypotension in older adults. The cardiovascular health study. CHS Collaborative Research Group. Hypertension 1992;19:508–519. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Arbogast SD, Alshekhlee A, Hussain Z, et al. Hypotension unawareness in profound orthostatic hypotension. Am J Med. 2009;122:574–580. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Hollister AS. Orthostatic hypotension: causes, evaluation, and management. West J Med. 1992;157:652–657. [PubMed], [Google Scholar]
- Shibao C, Lipsitz LA, Biaggioni I. Evaluation and treatment of orthostatic hypotension. J Am Soc Hypertens. 2013;7:317–324. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Williams B, Mancia G, Spiering W, et al. Practice guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC). Blood Press. 2018;27:314–340. [Taylor & Francis Online], [Web of Science ®], [Google Scholar]
- Cremer A, Rousseau AL, Boulestreau R, et al. Screening for orthostatic hypotension using home blood pressure measurements. J Hypertens. 2019;37:923–927. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Gorelik O, Cohen N. Seated postural hypotension. J Am Soc Hypertens. 2015;9:985–992. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Cooke J, Carew S, O'Connor M, et al. Sitting and standing blood pressure measurements are not accurate for the diagnosis of orthostatic hypotension. QJM 2009;102:335–339. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Fleg JL, Evans GW, Margolis KL, et al. Orthostatic hypotension in the ACCORD (Action to Control Cardiovascular Risk in Diabetes) blood pressure trial: prevalence, incidence, and prognostic significance. Hypertension 2016;68:888–895. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Parati G, Stergiou G, O’Brien E, et al. European Society of Hypertension practice guidelines for ambulatory blood pressure monitoring. J Hypertens. 2014;32:1359–1366. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Stuebner E, Vichayanrat E, Low DA, et al. Twenty-four hour non-invasive ambulatory blood pressure and heart rate monitoring in Parkinson’s disease. Front Neurol. 2013;4:49. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Voichanski S, Grossman C, Leibowitz A, et al. Orthostatic hypotension is associated with nocturnal change in systolic blood pressure. Am J Hypertens. 2012;25:159–164. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Costa A, Bosone D, Ramusino MC, et al. Twenty-four-hour blood pressure profile, orthostatic hypotension, and cardiac dysautonomia in elderly type 2 diabetic hypertensive patients. Clin Auton Res. 2016;26:433–439. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Vichayanrat E, Low DA, Iodice V, et al. Twenty-four-hour ambulatory blood pressure and heart rate profiles in diagnosing orthostatic hypotension in Parkinson's disease and multiple system atrophy. Eur J Neurol. 2017;24:90–97. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Norcliffe-Kaufmann L, Kaufmann H. Is ambulatory blood pressure monitoring useful in patients with chronic autonomic failure? Clin Auton Res. 2014;24:189–192. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Liyanage-Don N, Fung D, Phillips E, et al. Implementing home blood pressure monitoring into clinical practice. Curr Hypertens Rep. 2019;21:14. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Mehagnoul-Schipper DJ, van Kraaij DJ, Jansen RW. Achieving haemodynamic baseline values with Finapres in elderly subjects during supine rest. Clin Physiol. 2000;20:466–473. [Crossref], [PubMed], [Google Scholar]
- Cohen G, Zalomonson S, Press Y. Prevalence of orthostatic hypotension in the unselected ambulatory population of persons aged 65 years old and above. Blood Press. 2015;24:298–305. [Taylor & Francis Online], [Web of Science ®], [Google Scholar]
- Gorelik O, Feldman L, Cohen N. Heart failure and orthostatic hypotension. Heart Fail Rev. 2016;21:529–538. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Gorelik O, Almoznino-Sarafian D, Litvinov V, et al. Seating-induced postural hypotension is common in older patients with decompensated heart failure and may be prevented by lower limb compression bandaging. Gerontology 2009;55:138–144. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Finucane C, Savva GM, Kenny RA. Reliability of orthostatic beat-to-beat blood pressure tests: implications for population and clinical studies. Clin Auton Res. 2017;27:31–39. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Van Wijnen VK, Finucane C, Harms MPM, et al. Noninvasive beat-to-beat finger arterial pressure monitoring during orthostasis: a comprehensive review of normal and abnormal responses at different ages. J Intern Med. 2017;282:468–483. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Van Wijnen VK, Hove DT, Finucane C, et al. Hemodynamic mechanisms underlying initial orthostatic hypotension, delayed recovery and orthostatic hypotension. J Am Med Dir Assoc. 2018;19:786–792. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]
- Whelton PK, Carey RM, Aronow WS, et al. ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/ NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines. J Am Coll Cardiol. 2018;71:e127–e248. [Crossref], [PubMed], [Web of Science ®], [Google Scholar]