Normal cardiovascular responses to postural challenge

In the upright position gravity exerts a downward force on our bodies. This draws blood downward, creating a gradient in perfusion pressures to organs and tissues.Reference Smit, Halliwill, Low and Wieling^29, Reference Low³⁰ To maintain perfusion, a series of compensatory neuronal, humoral and endothelial mechanisms adapt HR, stroke volume, cardiac contractility, vascular resistance and venous capacitance.Reference Mathias and Bannister³¹

On standing upright after a period of recumbency there is displacement of 300–1000 ml of blood into the veins of the legs, pelvis and abdomen.Reference Smit, Halliwill, Low and Wieling^29, Reference Grubb³² This displacement is initially rapid, predominantly occurring within the first 10 seconds, although further accumulation continues over 3–5 minutes, with the majority of the redistribution occurring in the pelvic and upper leg veins.Reference Smit, Halliwill, Low and Wieling²⁹ Subsequently there is increased capillary filtration and a reduction in plasma volumeReference Smit, Halliwill, Low and Wieling^29, Reference Grubb³² and continuing transcapillary losses approach a steady state after 20–30 minutes.Reference van Lieshout, Wieling, Karemaker and Secher³³

Early after attaining an upright posture there is a reduction in venous return to the heart by 25–30%, leading to a transient reduction in stroke volume of approximately 40%Reference Smit, Halliwill, Low and Wieling^29, Reference Grubb³² following an initial brief delay due to the blood volume already within the thorax.Reference Low³⁰ To maintain cardiac output there is an acute compensatory increase in HR, systemic vascular resistance and venous tone.Reference Smit, Halliwill, Low and Wieling^29–Reference Mathias and Bannister^31, Reference Ewing, Campbell, Murray, Neilson and Clarke³⁴ These rapid changes are primarily mediated by the autonomic nervous system via sympatho-excitatory neurones under the influence of the carotid and aortic (high pressure) and pulmonary and cardiac (low pressure) baroreceptors.Reference Mathias, Bannister, Bannister and Mathias^10, Reference Smit, Halliwill, Low and Wieling²⁹

Also, as pressure rises, axonal reflexes lead to prompt increases in local smooth muscle tone acting on arteriolar and venous beds, with subsequent redistribution of blood flow.Reference Smit, Halliwill, Low and Wieling^29, Reference Low³⁰ In the steady state, these neuronal systems are in a state of continuous activation and have a periodicity that can also be used to differentially assess the functioning of the sympathetic and parasympathetic systems.Reference Mathias and Bannister^{31, 35}

Whilst neuronal control mechanisms are the key to effective cardiovascular responses to initial posture change, hormonal systems have increasing relevance with longer periods of orthostasis.Reference Low^30, Reference Mathias and Bannister³¹ Notably, in the setting of hypovolaemia, these hormonal fluxes are greater and occur earlier, augmenting the initial phases of postural cardiovascular control.Reference Low³⁰

Following orthostatic challenge, the adrenergic and renin-angiotensin-aldosterone systems are activated, contributing to the maintenance of plasma volume.Reference Mathias and Bannister^31, Reference Millet, Custaud, Maillet, Allevard, Duvareille, Gauquelin-Koch, Gharib and Fortrat³⁶ Systemic catecholamine levels have been seen to rise within minutes of postural change, whilst changes in renin-angiotensin-aldosterone are more gradual.Reference Low^30, Reference Mathias³⁷ Ordinarily, little change is seen in anti-diuretic hormone (ADH) levels unless hypotension develops, when there is a marked increase.Reference Low³⁰

Natriuretic peptides are released in response to stimulation from stretch receptors; these agents have diverse effects and sites of action, and a moderate influence on the activity of the adrenergic and renin-angiotensin-aldosterone systems.Reference Smit, Halliwill, Low and Wieling^29, Reference Akashi, Springer, Lainscak and Anker³⁸

Thus there are three distinct phases of normal postural cardiovascular control mechanisms; the first is the initial response related to early volume redistribution and neuronal control systems (about 0–30 s), followed by early steady state related to stabilization of neuronal mechanisms with early hormonal fluxes (about 1–2 min), and finally, during prolonged orthostasis, there is an ongoing maintenance phase of control and increasing hormonal input (about 5+ min).Reference Low³⁰

These mechanisms therefore combine to maintain tissue perfusion. Where there is failure of homeostatic mechanisms it is the cerebral circulation that is most vulnerable, leading to a variety of symptoms including visual disturbances and syncope.Reference Moya, Sutton and Ammirati¹⁹

Physiological measurements following orthostasis

Following orthostasis there is a normal transient increase in HR of 10–15 beats per minute, which is maximal about 15 heartbeats after standing.Reference Ewing, Campbell, Murray, Neilson and Clarke³⁴ This normal, prompt physiological response helps facilitate the maintenance of cerebral perfusion and systemic blood pressure. Its presence is an indicator of a functioning parasympathetic autonomic nervous system, is usually transient and is followed by a period of relative bradycardia (assessed by the 30:15 ratio).Reference Ewing and Clarke^20, Reference Ewing, Campbell, Murray, Neilson and Clarke³⁴ Furthermore, the lack of an initial HR rise in the setting of OH may aid in the identification of patients with a likely neurogenic mechanism.Reference Gupta and Nair³⁹

In contrast, in some patients, postural change is associated with excessive increases in HR and with a variety of symptoms including dizziness, visual disturbance, syncope and occasionally falls.Reference Jacob, Costa, Shannon, Robertson, Wathen, Stein, Biaggioni, Ertl, Black and Robertson^26, Reference Low^30, Reference Grubb³² Where there is a 30 beats per minute increment in HR whilst standing, this is suggestive of the condition Postural Orthostatic Tachycardia Syndrome (POTS).Reference Low^30, Reference Grubb^32, Reference Mathias⁴⁰ POTS is associated with a number of medical conditions (e.g. peripheral neuropathy, chronic fatigue syndrome) and muscular deconditioning (Table 1). The underlying mechanisms may include a partial denervation of the autonomic system with the lower limbs specifically involved, an elevation in adrenergic activity on gaining upright postureReference Jacob, Costa, Shannon, Robertson, Wathen, Stein, Biaggioni, Ertl, Black and Robertson^26, Reference Low³⁰ and/or disordered central HR control.Reference Grubb³² POTS may be overlooked if HR is not recorded during postural cardiovascular assessment and can be an early finding in the development of more widespread autonomic failure.Reference Low^30, Reference Jacob, Shannon, Black, Biaggioni, Mosqueda-Garcia, Robertson and Robertson⁴¹

Table 1.

Classification of OH and related conditions, adapted from Moya et al. 2009Reference Moya, Sutton and Ammirati¹⁹

CO, cardiac output; SVR, systemic vascular resistance; VR, venous return; CSS, carotid sinus syndrome.

Definition of orthostatic hypotension

The most commonly applied definition is that OH is present where there is a drop in systolic blood pressure of 20 mmHg or more, and/or in diastolic blood pressure of 10 mmHg or more, occurring within the first three minutes of standing (or during head-up tilt-table testing). This consensus definition was published in 1996 by the American Autonomic Society and the American Academy of Neurology (AAS/AAN).^42, Reference Kaufmann⁴³ Prior to this there had been inconsistency, with marked variation in definitions used.Reference Ewing and Clarke^20, Reference Low^30, Reference Atkins, Hanusa, Sefcik and Kapoor⁴⁴

The consensus statement also highlights that some patients manifest hypotension 10 minutes or more after standing and therefore it is suggested, where clinical suspicion is high and initial testing is negative, that repeated and extended measurements are warranted.⁴²

Although generally accepted, the consensus definition of OH as a BP reduction of 20/10 mmHg is arbitrary.Reference Mathias^37, Reference Carey and Potter^45, Reference Weiss, Chagnac, Beloosesky, Weinstein, Grinblat and Grossman⁴⁶ Symptomatic hypotension can occur with blood pressure changes at levels less than this,Reference Mathias^37, Reference Weiss, Chagnac, Beloosesky, Weinstein, Grinblat and Grossman^46–Reference Carlson⁴⁸ particularly where there is relative baseline hypotension or obstruction to cerebral blood flow.Reference Mathias and Bannister³¹ Furthermore, OH was found to be associated with mortality in a linear fashion in the Honolulu heart study, without evidence of a threshold level.Reference Masaki, Schatz, Burchfiel, Sharp, Chiu, Foley and Curb¹² Given this and the overall weak association found in many studies between OH and clinical outcomes, some authors have suggested that a review of the AAS/AAN diagnostic criteria would be appropriate.Reference Belmin, Abderrhamane, Medjahed, Sibony-Prat, Bruhat, Bojic and Marquet^8, Reference Weiss, Chagnac, Beloosesky, Weinstein, Grinblat and Grossman^46, Reference Caine, Alsop and MacMahon⁴⁹

The 2009 European Society of Cardiology (ESC) syncope guidelines seek to further refine the characterization of OH (Table 1).Reference Moya, Sutton and Ammirati¹⁹ In this updated guidance OH is subdivided into initial (occurring within 30 s), classical (30 s to 3 min) and delayed (progressive; which occurs after 3 min). These phases have a logical relationship with the mechanisms involved in the maintenance of blood pressure, and act to reinforce the necessity for the recording of serial measurements of BP in the assessment of postural cardiovascular responses. At present, such subdivisions may suggest differential underlying mechanisms but recommended interventions are not differentiated.Reference Moya, Sutton and Ammirati¹⁹

Delayed OH is characterized by a gradual progressive fall in BP, whereas with vasovagal syncope, the typical pattern is of an abrupt change, with or without an associated reduction in heart rate.Reference Moya, Sutton and Ammirati¹⁹ It is the gradual nature of the BP fall and the absence of changes in HR that help differentiate delayed OH from vasovagal syncope (Table 1).Reference Moya, Sutton and Ammirati¹⁹

In establishing the relevance of a diagnosis of OH it should be noted that the changes in blood pressure seen are often inconsistent and the finding of OH may not be a reliable finding. Where the finding is more consistent and associated with symptoms, it is more likely to be clinically relevant.Reference Ooi, Barrett, Hossain, Kelley-Gagnon and Lipsitz²¹ Where patients have symptoms associated with postural change and a degree of hypotension develops that does not meet these thresholds, it is relevant for clinicians to consider this. The diagnostic label of symptomatic postural hypotension may be preferable in such circumstances, but it is prudent to ensure the presence or absence of symptoms is recorded during assessment as a matter of routine.

In patients who have a marked HR rise on standing without evidence of intravascular volume depletion, a diagnosis of POTS should be considered. This is often associated with pronounced symptoms including chest pain, dizziness and fatigue.Reference Carlson⁴⁸

Isolated diastolic orthostatic hypotension

Although the importance of systolic OH is generally accepted and established in relation to falls and symptoms of cerebral hypoperfusion, the significance of isolated diastolic OH, which is less common, is not agreed.Reference Luukinen, Koski, Laippala and Kivela^4, Reference Weiss, Grossman, Beloosesky and Grinblat^6, Reference Tilvis, Hakala, Valvanne and Erkinjuntti^14, Reference Ward and Kenny^22, Reference Brignole, Alboni and Benditt^47, Reference Eigenbrodt, Rose, Couper, Arnett, Smith and Jones⁵⁰ The evidence that diastolic hypotension relates to cerebral hypoperfusion or volume depletion is debated, although there are consistent associations with vascular diseases and mortality.Reference Tilvis, Hakala, Valvanne and Erkinjuntti^14, Reference Eigenbrodt, Rose, Couper, Arnett, Smith and Jones⁵⁰

Symptoms in orthostatic hypotension

OH may present with postural dizziness, visual/auditory disturbance, presyncope, syncope or seizures, although symptoms are often milder in older patients than in younger ones and may be absent, even when hypotension is marked.Reference Atkins, Hanusa, Sefcik and Kapoor^44, Reference Carlson^48, Reference Arbogast, Alshekhlee, Hussain, McNeeley and Chelimsky⁵¹ Numerous other less common symptoms have also been reported and include chest pain, the characteristic ischaemic neck/shoulder (‘coat-hanger’) pain, buttock/thigh pain, nausea, palpitations, dyspnoea, episodic confusion, intermittent focal neurological symptoms and non-specific malaise.Reference Mathias^{40, 42,} Reference Arbogast, Alshekhlee, Hussain, McNeeley and Chelimsky^51–Reference Gibbons and Freeman⁵³

Whilst in the interpretation of the finding of OH the presence of symptoms (or the development of postural instability or body sway) is helpful, the absence of symptoms does not necessarily indicate a non-significant clinical finding.^42, Reference Brignole, Alboni and Benditt^47, Reference Carlson⁴⁸ In older subjects up to 30% with significant OH may be asymptomatic, whilst a further 24% may have atypical symptoms.Reference Arbogast, Alshekhlee, Hussain, McNeeley and Chelimsky⁵¹

Causes of orthostatic hypotension

Although OH can be due to a wide variety of conditions (see Table 2), in older people OH is frequently multifactorial; common contributing factors include underlying medical conditions, drug treatments, sarcopenia, blunted hormonal responses, reduced adrenoreceptor and baroreceptor sensitivity and impaired volume regulation.Reference Atkins, Hanusa, Sefcik and Kapoor^44, Reference Carlson^48, Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari⁵²

Table 2.

Selected causes of orthostatic hypotension

Hypertension is a risk factor for the development of OH.Reference Fedorowski, Stavenow, Hedblad, Berglund, Nilsson and Melander¹ When OH occurs in patients with supine hypertension, defining the optimal BP management can be extremely challenging.Reference Mathias and Bannister^31, Reference Brignole, Alboni and Benditt^47, Reference Shibao, Gamboa, Diedrich and Biaggioni⁵⁴ There is evidence that OH is a consequence of impaired baroreceptor function, and that by improving control of hypertension there may be an improvement in OH.Reference Naschitz, Slobodin, Elias and Rosner⁵⁵ This approach must be balanced against the risk of worsening OH and clinical sequelae. The optimal treatment regime in these circumstances remains uncertain and a cautious approach is recommended.

Assessing postural cardiovascular responses

Unfortunately, whilst recommending the routine measurement of postural blood pressure as a technique for identifying OH, many of the key guidelines do not offer specific advice on the active stand technique, the most suitable method for routine clinical assessment.^{16, 42,} Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari^{52, 56} Where advice is available, it is at times inconsistent and conflicting.Reference Low^30, Reference Mathias and Bannister^31, Reference Kenny^57, Reference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG⁵⁸ The lack of consistent advice and guidance on the measurement of OH by the active stand method, in contrast with tilt-table testing, is explained by the limited research base upon which evidence can be directly drawn.Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari⁵²

Recommended techniques in the literature

The consensus report of the AAS/AAN⁴² does not give explicit details in the measurement techniques for the detection of OH, and previous reviewers have noted a continuing concern about how best to assess OH using the active stand technique.Reference Carey and Potter^45, Reference Carlson⁴⁸

The European Federation of Neurological Societies’ guidelines for the ‘Diagnosis and Management of OH’ recommend initially assessment of BP and HR whilst supine and for up to 3 minutes whilst standing. Further recommendations are not given although testing with passive head-up tilt-table testing (HUTT) is advised using a specified protocol.Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari⁵²

A period of rest before BP measurement is recommended for all routine readings.Reference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG^58, Reference Chobanian, Bakris and Black⁵⁹ Most guidance recommends a minimum 5 minute period of rest. Lance et al.Reference Lance, Link, Padua, Clavell, Johnson and Knebel⁶⁰ studied the measurement of supine BPs in healthy volunteers at 5, 10 and 15 minutes. After 5 minutes supine rest average BP was 113.8/62.6; however, a further reduction occurred over the following 5 minutes with BP at 10 minutes showing no difference to BP at 15 minutes (109.3/60.3 vs. 109.4/59.5). No changes in HR were seen with duration of rest.

As described above, the maintenance of BP is under complex control. Humoral systems are much slower to adapt to postural changes and therefore Mathias & BannisterReference Mathias and Bannister³¹ advised that an optimal duration of rest before study is at least 20 minutes, whilst acknowledging that this may not be practical in routine clinical work.

Fealey & Robertson (quoted by LowReference Low³⁰) recommend a 2 minute period of measurement with recording made of BP and HR using a cuff sphygmomanometer, stating that this should be preceded by 2 minutes of supine rest. KennyReference Kenny⁵⁷ also recommends a 2 minute measurement period with a rest period advised of 15 minutes.

Through the use of continuous BP monitors, authors have been able to study closely the patterns of BP response to postural change. The nadir of BP is usually seen at approximately 1–1½ minutes, with a subsequent period of recovery.Reference Ward and Kenny^22, Reference Atkins, Hanusa, Sefcik and Kapoor⁴⁴ However, this is not a universal finding and other patterns are recognized.Reference Moya, Sutton and Ammirati^19, Reference Gibbons and Freeman^53, Reference Macrae and Bulpitt⁶¹

Although some authors suggest a single orthostatic measurement of BP, usually to be performed at 1 or 2 minutes, this approach reduces both the sensitivity and reproducibility of measurements and may fail to capture the nadir.Reference Belmin, Abderrhamane, Medjahed, Sibony-Prat, Bruhat, Bojic and Marquet^{8, 16,} Reference Caine, Alsop and MacMahon⁴⁹ In contrast, the use of continuous BP monitoring systems has been shown to increase the sensitivity of postural BP responses, but such equipment is not routinely available and requires greater time and expertise to use.Reference Ward and Kenny^22, Reference Mathias and Bannister^31, Reference Caine, Alsop and MacMahon⁴⁹

The ESC guidelines suggest that repeated measurements of BP are made over 3 minutes and longer if minor degrees of hypotension are found or if hypotension is progressing.Reference Brignole, Alboni and Benditt⁴⁷ They recommend also that either a manual sphygmomanometer or continuous beat-to-beat system is used in the performance of BP measurements. The manual technique can be used to monitor BP changes more closely and allows skilled practitioners to track changes in BP.Reference Moya, Sutton and Ammirati¹⁹ Using the manual technique, a skilled operator can perform up to three measurements per minute, although venous occlusion can occur.

Fundamental to the accurate recording of postural BP are the generic skills of BP measurement. Adherence to the principles of practice outlined in the British Hypertension Society (BHS) guidance are therefore strongly recommended (e.g. arm position, the selection of the correct cuff size and its location on the arm, loosening of tight clothing, maintenance of equipment).Reference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG⁵⁸ Nevertheless, physicians’ compliance with such recommendations has been found to be poor.Reference McKay, Campbell, Parab, Chockalingam and Fodor²⁵ Furthermore, where BP readings are made by different individuals using manual sphygmomanometers, there is increased variability in the measured BP.Reference Gorny^62, Reference McAlister and Straus⁶³

In contrast, concerns have been raised that many automated sphygmomanometers are not validated for the measurement of BP in patients with significant rhythm disturbances (e.g. atrial fibrillation or with frequent ectopics). Additionally, these systems may fail to record (or delay reading) BPs in situations of low flow (e.g. hypotension) or where there are marked changes or instability in BP; therefore they represent a risk when used for postural BP measurements.Reference Moya, Sutton and Ammirati^19, Reference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG^58, Reference Gorny⁶²

The use of sitting to standing measures would simplify the assessment of postural cardiovascular responses in many clinical settings. This is recommended by some authorsReference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG⁵⁸ and is often observed during routine practice.Reference Cooke, Carew, O'Connor, Costelloe, Sheehy and Lyons²⁴ The use of the seated position for recording BP has been investigated and compared with the supine.Reference Cooke, Carew, O'Connor, Costelloe, Sheehy and Lyons^24, Reference Netea, Smits, Lenders and Thien⁶⁴ Whilst resting supine and seated BP measurements are well correlated, particularly in the elderly,Reference Netea, Smits, Lenders and Thien⁶⁴ the correlation with subsequent measurements after orthostasis is poor. Cooke et al.Reference Cooke, Carew, O'Connor, Costelloe, Sheehy and Lyons²⁴ found only a 16% sensitivity when compared with tilt-table test findings. However, whether OH detected from the seated position is more (or less) sensitive than measurements from supine in terms of clinical outcomes is not established.

Overall, active stand techniques for assessment of orthostatic cardiovascular responses have been shown to be safe, although appropriate manual handling techniques do need to be applied, especially when the procedure is undertaken with a frail, confused patient or when the possibility of resultant syncope is high (e.g. severe autonomic failure).

In some patients a measurement of postural BP may be required immediately at the time of presentation (e.g. in the emergency department or out-patient clinic), whilst in others the measurement can be elective and procedures to ensure optimal recording circumstances can be applied.

Factors influencing postural cardiovascular measurements

BP and HR vary in response to physical activity, emotional and psychological factors, pharmacological agents, dietary and fluid intake and to many chemical stimuli.Reference Vloet, Pel-Little, Jansen and Jansen^5, Reference Brignole, Alboni and Benditt^47, Reference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG⁵⁸ Intra-individual findings of OH vary significantly throughout the day by a standard deviation of 12/8 mmHg.Reference McAlister and Straus⁶³ Weiss et al.Reference Belmin, Abderrhamane, Medjahed, Sibony-Prat, Bruhat, Bojic and Marquet⁸ found OH to be most prevalent in the early afternoon when studied in hospital in-patients. However, other authors have reported prevalence of OH to be greatest in the morning.Reference Gorelik, Fishlev, Litvinov, Almoznino-Sarafian, Alon, Shteinshnaider, Chachashvily, Modai and Cohen^7, Reference Belmin, Abderrhamane, Medjahed, Sibony-Prat, Bruhat, Bojic and Marquet^8, Reference Ward and Kenny^22, Reference Macrae and Bulpitt⁶¹ Gorelik et al.Reference Gorelik, Fishlev, Litvinov, Almoznino-Sarafian, Alon, Shteinshnaider, Chachashvily, Modai and Cohen⁷ studied 121 hospital in-patients and found a particularly high incidence (64.5%) of OH on first rising in the morning, using intermittent measurements and recording BP at 1, 3 and 5 minutes; patients spending longer than 8 hours in bed were at significantly increased risk (P < 0.001).

Whilst some studies have found greater reproducibility in the morning,Reference Vloet, Pel-Little, Jansen and Jansen^5, Reference Weiss, Grossman, Beloosesky and Grinblat^6, Reference Ward and Kenny²² other authors have not.Reference Belmin, Abderrhamane, Medjahed, Sibony-Prat, Bruhat, Bojic and Marquet⁸ Post-prandial hypotension is a common finding in frail older people (38–67%) and is considered distinct from OH.Reference Vloet, Pel-Little, Jansen and Jansen^5, Reference Weiss, Grossman, Beloosesky and Grinblat^6, Reference Fisher, Davis, Srikusalanukul and Budge⁶⁵ Yet post-prandial orthostatic BP measurements identify a number of patients who do not demonstrate OH at other times.Reference Vloet, Pel-Little, Jansen and Jansen^5, Reference Weiss, Grossman, Beloosesky and Grinblat^6, Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari⁵²

Overall reproducibility of orthostatic hypotension in trials

Authors have noted that the finding of OH following an active stand remains inconsistent, with poor reproducibility.Reference Alli, Avanzini and Bettelli^2, Reference Weiss, Chagnac, Beloosesky, Weinstein, Grinblat and Grossman⁴⁶ For authors studying subjects at the same time of day with standardized methodology there still remains a lack of consistency in the finding of OH, with only about one-third of patients showing reproducible findings.Reference Alli, Avanzini and Bettelli^2, Reference Belmin, Abderrhamane, Medjahed, Sibony-Prat, Bruhat, Bojic and Marquet^8, Reference Ward and Kenny²² Where patients have a consistent finding of OH this has been shown to be more strongly associated with falls.Reference Ooi, Barrett, Hossain, Kelley-Gagnon and Lipsitz²¹ Thus demonstrating a lack of reproducibility may in itself be clinically relevant.

The reproducibility of postural cardiovascular responses is improved by the use of standardized tilt-table testing using continuous beat-to-beat BP monitoring when compared with intermittent measurements using the active stand technique.Reference Gabbett and Gass⁶⁸ However, this technique is relatively complex, requiring specialist equipment, and is not widely available for routine clinical measurement. It is, however, considered the reference standard for assessment of OH.Reference Cooke, Carew, O'Connor, Costelloe, Sheehy and Lyons^24, Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari⁵² However, HUTT is a passive process of orthostasis and, as such, the mechanisms involved in maintaining cardiovascular homeostasis are subtly different from a ‘normal’ active stand.Reference Cooke, Carew, O'Connor, Costelloe, Sheehy and Lyons^24, Reference Kenny⁵⁷ Thus although studies using the HUTT approach to assess postural cardiovascular responses are instructive, there is the potential for the finding to be less clinically relevant than measurements by the active stand methodology.Reference Cooke, Carew, O'Connor, Costelloe, Sheehy and Lyons^24, Reference Kenny⁵⁷

In summary, the recommendations on the measurement procedure for investigation of OH by active stand technique in standard reference texts and papers show significant variation. Thus it is not possible to identify a consensus approach or best practice outline solely from such sources.

Recommendations (Table 3)

There is a lack of scientific studies comparing various aspects of the active stand methodology in the assessment of orthostatic cardiovascular responses and specific long-term clinical outcomes.Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari⁵² This has resulted in the development of varied measurement protocols seen in both the clinical setting and published literature. Such varied measurement protocols further contribute to the complexity of study analysis and in comparing the individual studies.Reference Ward and Kenny^22, Reference Lahrmann, Cortelli, Hilz, Mathias, Struhal and Tassinari⁵²

Table 3.

Recommendations for assessing orthostatic hypotension

It is notable that the use of automated BP measurement systems is now commonplace in the published literature as well as in clinical practice. It is also noteworthy that not all available systems are validated to the standards of the BHS (a list of validated systems can be accessed on the BHS website: www.bhsoc.org/bp_monitors/automatic_clinic.stm). As automated devices often set a target BP related to previous readings, where there are large changes in BP, the devices take longer, or repeat, measurements. In situations of low flow such devices may be unable to measure the BP; therefore, where there are significant changes in BP such devices may fail or delay readings and thus they are not recommended for the measurement of orthostatic hypotension.Reference Moya, Sutton and Ammirati¹⁹

The use of a manual sphygmomanometer can allow the experienced practitioner to undertake repeated assessments quickly. It does, however, require training and development of a skill base. Although the skills of BP measurement are considered a fundamental tool for both doctors and nurses, studies looking at the application of these skills in clinical practice have identified poor procedures and multiple errors.Reference McKay, Campbell, Parab, Chockalingam and Fodor^25, Reference McAlister and Straus^63, Reference Vloet, Smits, Frederiks, Hoefnagels and Jansen⁶⁹

Continuous beat-to-beat monitoring systems have been recommended in the measurement of postural cardiovascular measurements.Reference Mathias and Bannister^31, Reference Kenny⁵⁷ These systems do, however, require greater technical skill and are more costly in terms of initial outlay, maintenance and repairs. They have the advantage that continuous monitoring systems allow uninterrupted recordings of the BP and HR. Studies have demonstrated that the use of such systems improves the identification of episodes of transient OH.Reference Ward and Kenny^22, Reference Van Der Velde, Van Den Meiracker, Stricker and Van Der Cammen⁷⁰ However, whether brief episodes of asymptomatic hypotension detected on standing by beat-to-beat systems carry the same implications to those detected by traditional methods is uncertain.Reference Van Der Velde, Van Den Meiracker, Stricker and Van Der Cammen⁷⁰ The training and investment in equipment that would be required for widespread use of beat-to-beat BP systems is substantial.

The most widely applicable technique for measurement of postural cardiovascular responses is therefore through the use of manual equipment that is appropriately maintained, and is performed by staff who are adequately trained. The use of automated devices, which is now widespread, carries a small risk that the devices will fail to detect significant OH. As long as staff appreciate this and pay close attention to the patient during the measurement period, the attendant risk is low; and this theoretical concern was not highlighted in the studies that used such devices. No matter what approach is used, staff should be performing to the standards of BP measurement as laid down in the BHS guidelines.Reference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG^58, Reference McAlister and Straus⁶³

A very high incidence of OH has been demonstrated initially on rising (in the morning) in hospital in-patients, with a high symptom frequency, whilst others have found the peak to be later in the morning.Reference Gorelik, Fishlev, Litvinov, Almoznino-Sarafian, Alon, Shteinshnaider, Chachashvily, Modai and Cohen^7, Reference Ward and Kenny²² Where orthostatic BP measurement is to be undertaken first thing in the morning, this should be before there is significant physical activity. Additionally, some patients have symptomatic OH only post-prandially, and thus detection requires clinical suspicion and measurements after meal times. Whilst for some patients (e.g. hospital in-patients) there is flexibility in the timing of postural cardiovascular measurements, this is not the case for many clinical encounters (e.g. emergency unit, out-patient clinics).

The performance of seated to standing BP is not optimal, and this approach should only be considered when there is no alternative. Although it can be useful and does identify some patients with marked OH, it is a significant compromise with a high rate of false negatives.Reference Cooke, Carew, O'Connor, Costelloe, Sheehy and Lyons^24, Reference Carlson^48, Reference Netea, Smits, Lenders and Thien⁶⁴

The optimal period of supine rest that should precede a measurement of OH is not defined; it is recommended that all patients have a period of 5 minutes supine rest before measurements are made, in keeping with the JNC and BHS guidelines, although a supine rest period of 10 minutes may offer an advantage.Reference Williams, Poulter, Brown, Davis, McInnes, Potter, Sever and McG^58, Reference Chobanian, Bakris and Black^59, Reference Lance, Link, Padua, Clavell, Johnson and Knebel⁶⁰ The use of a single measurement approach has been shown to fail to identify many patients with OH when compared with continuous measurement systemsReference Ward and Kenny^22, Reference Caine, Alsop and MacMahon⁴⁹ or repeated intermittent readings.Reference Luukinen, Koski, Laippala and Kivela^4, Reference Belmin, Abderrhamane, Medjahed, Sibony-Prat, Bruhat, Bojic and Marquet⁸ BP should be recorded immediately on standing and repeated over the following 3 minutes.

Whether the recording period need be as long as 30 minutes or more, as suggested by some authors, is not proven.Reference Cheshire and Phillips⁷¹ Given the lack of evidence and resource implications for such a period, it is not recommended that the measurement time is extended beyond 5 minutes in routine clinical settings.

Although uncommon, the finding of orthostasis related sinus tachycardia (HR rise increase 30 beats per minute) is significant and suggestive of POTS.Reference Low^30, Reference Grubb^32, Reference Mathias⁴⁰ Furthermore, patients with OH who do not have a HR rise (in the absence of rate-limiting medication) are more likely to have a neurogenic aetiology, and therefore recording the pulse rate can assist in guiding further investigations as to the cause of OH.Reference Gupta and Nair³⁹

As has been discussed, the finding of OH in older people is extremely common. Potentially important features in its analysis are the degree of drop in BP, associated changes (or lack of) in heart rate, and the presence of signs and symptoms and the consistency of the finding. It is important therefore that symptoms are identified and actively sought by directly asking the patient about them.Reference Carlson⁴⁸ However, as there is a large subpopulation (30%) with marked OH who do not report symptoms, a high index of suspicion should be applied.Reference Arbogast, Alshekhlee, Hussain, McNeeley and Chelimsky⁵¹

Conflicts of interest

The author has no conflicts of interest to declare.