Author + information
- Received February 2, 2005
- Revision received May 31, 2005
- Accepted June 6, 2005
- Published online October 4, 2005.
- Victoria E. Claydon, PhD⁎ ( and )
- Roger Hainsworth, MB, PhD, DSc
- ↵⁎Reprint requests and correspondence:
Dr. Victoria E. Claydon, Institute for Cardiovascular Research, University of Leeds, Leeds, LS2 9JT, United Kingdom
Objectives This study sought to evaluate postural sway in control subjects with good and poor orthostatic tolerance (OT).
Background Some asymptomatic volunteers, when subjected to a progressive orthostatic stress test, show early presyncope. We hypothesized that normal subjects with poor OT do not usually faint because they adopt a strategy of increased lower limb movement, which helps maintain venous return.
Methods In 12 asymptomatic subjects with good OT and 11 with poor OT, assessed by the combined orthostatic stress of head-up tilting and lower body suction, we determined postural sway using a force platform after 1, 5, and 10 min of motionless standing.
Results The subjects with poor tolerance had greater distances and velocities of sway in the anteroposterior direction but not the mediolateral direction. There was a significant negative correlation between postural sway and orthostatic tolerance.
Conclusions We have shown that in normal subjects with poor OT during a passive orthostatic stress test, their leg movements tend to be greater when standing. These movements are likely to enhance venous return and may at least partly explain why, despite their poor test results, they do not normally faint.
Unexplained syncope is a common clinical problem (1). Patients with unexplained syncope are commonly investigated by head-up tilting, often with vasodilator agents (2,3). However, the use of such agents has the disadvantage that false-positive results may frequently be obtained in entirely asymptomatic subjects (4). We have extensive experience of a test that combines head-up tilting with lower body suction (5) and have found it to induce earlier presyncope in patients with convincing histories than in asymptomatic subjects (6). Nevertheless, there are some subjects who have never fainted but who have early syncope during this orthostatic stress test. This may be explained by the different stimulus provided by the orthostatic stress test compared with normal standing. Tilt testing minimizes the normal leg movements, and thus inactivates the skeletal muscle pump. During normal standing, however, postural muscles are continually reciprocally activated, and this would enhance venous return (7). Thus, our hypothesis is that asymptomatic subjects who never normally faint but who develop early syncope during orthostatic stress testing subconsciously adopt a strategy of increased leg movements to compensate for their poor tolerance. Subjects with good tolerance to orthostatic stress do not require excessive limb movements, so their postural sway is likely to be less.
Subjects were recruited from staff and students at Leeds University and the Leeds General Infirmary. All were apparently healthy and were taking no medication, and none had a history of fainting. All subjects gave written informed consent. The study was approved by the local Research Ethics Committee and was performed in accordance with the Declaration of Helsinki (2002) of the World Medical Association. Since it is uncommon for healthy, asymptomatic controls to have poor OT, control subjects with poor OT were identified from the control limb of research studies undertaken in our laboratory over the previous six years. They were then matched as closely as possible with control subjects with good OT. Subject characteristics can be seen in Table 1.
Tests were performed in the morning in a temperature-controlled laboratory (22°C to 24°C). Subjects abstained from alcohol and caffeine from the previous night and ate only a light breakfast. The orthostatic stress test was performed first, and then postural sway recordings were performed at least 24 h later.
Orthostatic stress test
Orthostatic tolerance (OT) was determined using combined head upright tilting and lower body suction (5). Briefly, while we monitored the electrocardiograph (Hewlett Packard 78325C, Boebringen, Germany) and blood pressure (Finapres, Ohmeda, Wisconsin), the subject rested supine for 20 min. The subject was then tilted by 60° for 20 min. Finally, while tilted, lower body suction was applied at −20 and −40 mm Hg for 10 min each, or until onset of presyncope (systolic pressure <80 mm Hg and symptoms of presyncope). The OT was assessed as time from the start of tilting until presyncope occurred. During the test, brachial artery blood flow velocity was determined using the Doppler technique (Multi-Dop X4, TCD-8.01, DWL Elektronische System GmbH, Sipplingen, Germany) (8). Forearm vascular resistance was calculated from blood pressure divided by blood flow velocity. Subjects were classified as having good or poor OT according to previously published predicted values (5).
Postural sway dynamics
A computerized biomechanics measuring system determined both distance and velocity of postural sway movements in the anteroposterior and mediolateral directions (AMTI force platform, model OR6-5-1, Advanced Mechanical Technology, Inc., Watertown, Massachusetts) (9,10). Subjects were instructed to stand still in a standardized position on the platform with their eyes open. There were no horizontal or vertical visual cues within the visual field, and no auditory cues. Measurements were performed for 30-s time periods after 1, 5, and 10 min of motionless standing.
Statistical analyses were performed using GraphPad Instat version 3.00 for Windows 95 (GraphPad Software, San Diego, California). Data are expressed as mean ± standard error of the mean. Comparisons between the two groups were performed using unpaired student ttests. Correlations between variables were performed using the Pearson correlation coefficient. Statistical significance was assumed at the level of p < 0.05.
OT and group characteristics
On the basis of their OT, subjects were divided into two groups as described in Table 1. As a result of prespecified matching, there were no significant differences in age or gender between the two groups. There were also no differences in height, weight, or body mass index between the two groups. By definition, those with good OT had significantly greater times to presyncope than those with poor OT (p < 0.001).
Cardiovascular responses to orthostatic stress
There were no significant differences in the supine systolic, diastolic, or mean arterial pressures between groups (mean arterial pressure: poor OT, 84.9 ± 2.4 mm Hg; good OT, 84.8 ± 3.0 mm Hg; not significant [NS]). Supine heart rates were also similar. Blood pressures at termination of the tests were also similar (good OT, 75.0 ± 3.8/47.6 ± 2.5 mm Hg; poor OT, 78.8 ± 2.7/42.1 ± 2.6 mm Hg; NS). Subjects with poor OT, however, developed smaller maximal increases in forearm vascular resistance (Fig. 1A).We also found a significant positive correlation between OT and the maximum vascular resistance response (R2= 0.428; R = 0.654; p < 0.001), whereby those individuals with the greatest OT showed the most powerful vasoconstriction (Fig. 1B).
The distance and velocity of movement in mediolateral and anteroposterior directions and the total distance or velocity of movement after 1, 5, and 10 min of standing can be seen in Table 2.The subjects with poor OT showed greater sway in all parameters than those with good OT. This was particularly apparent in the anteroposterior direction (Fig. 2).
We found a significant negative correlation between OT and distance moved anteroposteriorly (p < 0.05), total distance moved (p < 0.05), velocity moved anteroposteriorly (p < 0.05), and the mean velocity (p < 0.05) after 5 and 10 min of standing (Fig. 3).We also found a significant negative correlation between the maximum vascular resistance response and the distance and velocity of movement in the anteroposterior direction (p < 0.05) after five minutes of standing (Fig. 4).
Multiple regression analyses of OT with the maximum vascular resistance response and the parameters of postural sway showed that both vascular resistance (p < 0.01) and anteroposterior sway (both the velocity and distance moved, p < 0.05) after 10 min of standing were correlated with OT independently of each other.
We have shown for the first time that healthy individuals who do not normally faint, but who have poor OT during tilt testing, subconsciously adopt a strategy of increased leg movement during standing. The associated muscular contractions rhythmically compress leg veins and thereby maintain an adequate venous return (7). This would explain why, despite their tendency toward syncope at an early phase of tilt testing, control subjects with poor OT who show greater postural sway during normal standing do not normally faint.
In this study we assessed OT using combined head-up tilt and graded lower body suction. We have considerable experience with this technique, which is known to be sensitive and reproducible (5). It is also relatively specific, in that there is little overlap between time to presyncope of patients with histories of syncope and asymptomatic volunteers (6). The results of the present study may seem contradictory to the reported high sensitivity and specificity of this test. However, this is not the case. The subjects with poor OT in this study were recruited from a large pool of approximately 130 volunteers who had participated in the control limb of other research studies in our laboratory. This represents a specificity that is compatible with our earlier findings. Subjects with good OT were then selected in order to match, as closely as possible, the subject characteristics of this group of controls with poor OT.
The greater sway in the subjects with poor OT occurred mainly in the anteroposterior direction; mediolateral movements were similar. Mediolateral movements mainly involve thigh muscles, whereas anteroposterior movements are primarily attributable to antagonistic contraction of the calf muscles (11). Since the calf would be exposed to the greatest venous pressures when upright, the enhanced pumping by muscles in that region should have the greatest effect on venous return.
There are several possible reasons why our asymptomatic subjects might have a poor tolerance to the artificial orthostatic stress imposed by the test. We have previously shown that patients with poor OT have smaller increases in vascular resistance than normal subjects (8), and in this study, we also showed smaller resistance responses in the poor OT subjects. Another possibility is that those with poor OT may have smaller plasma and blood volumes, and these are also known to influence OT (12). However, what is unknown is how these subjects have “learned” to sway more during standing. Instructing patients who faint to increase muscle contraction in the legs and buttocks is an effective way of preventing such attacks (13). However, our subjects had not previously fainted and had not received any advice on voluntary muscle contractions. One possibility is that our subjects may be natural “swayers” and, because they do not normally stand still, less of a challenge is presented to blood pressure regulation, and consequently the regulatory mechanisms become less effective. Conversely, the increased postural sway in these individuals may be a compensatory mechanism to counteract their smaller reflex responses.
In the subjects with poor OT, sway tended to increase after five minutes of standing. This is important because one of the most common triggers for syncopal reactions is prolonged standing (14). The greater sway over time would presumably help to counteract the translocation of fluid to the lower limb vasculature that occurs in a time-dependent manner.
It is also noteworthy that individuals known to have an increased susceptibility to postural hypotension and syncope, such as patients with Alzheimer disease (15), patients suffering from the postural tachycardia syndrome (POTS) (16), or astronauts after prolonged space flight (17), show enhancement of postural sway. Furthermore, paraplegic and tetraplegic patients who are lacking this skeletal muscle pumping effect are prone to postural hypotension (18). Interestingly, electrically stimulated leg muscle contractions in these individuals prevent this orthostatic hypotension (18).
The measurement of postural sway is not an exact science and is subjected to a variety of influences. Postural control is thought to depend on the integration of visual, vestibular, proprioceptive, and auditory information (10,19,20), and may be influenced by various physical factors, including the subjects’ age, gender, weight, and height (21). Thus, the subject’s position was standardized, there were no visual or auditory cues, and physical factors were controlled.
We believe that, although our work makes an interesting and possibly relevant association, it does not establish proof that greater sway enhances venous return. Measurements of sway do show good within-subject reproducibility, (22), so differences between subjects are likely to be consistent. Nevertheless, we do not know from this study the exact magnitude of the effect of the recorded sway on venous return or on capillary transudation. However, Inamura et al. (23) reported that postural sway, similar to that observed in the present study, did limit the pooling of blood. It seems likely, therefore, that the degree of postural sway is an important factor in preventing posturally related syncope.
We have shown that healthy volunteers who do not normally faint but who have poor OT during tilt testing adopt a strategy of enhanced postural sway during normal standing. The increased leg movement would be likely to contribute to an enhancement of venous return, and this could explain why these individuals do not normally faint. We do not yet know the role of limb movements in patients who faint, but these results suggest that encouraging leg movement in such patients is likely to be of benefit.
We thank Professor Roger Soames, PhD, for providing access to his biomechanical force measuring platform during the course of this study.
- Abbreviations and Acronyms
- not significant
- orthostatic tolerance
- Received February 2, 2005.
- Revision received May 31, 2005.
- Accepted June 6, 2005.
- American College of Cardiology Foundation
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