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The control of blood pressure using pulse-wave velocity feedback
Journalof PsychosomaticResearch,Vol. 20, pp. 417 to 424. PergamonPress, 1976. Printedin Great Britain.
THE CONTROL OF BLOOD PRESSURE USING PULSE-WAVE VELOCITY FEEDBACK* ANDREW
STEPTOE AND
(Received
DEREK
2 January
JOHNSTON~’
1976)
SEVERAL studies of blood pressure (BP) control have recently been carried out using feedback from automated occlusion cuff measurement systems [I, 21. An alternative method for monitoring pressure is based on the relationship between changes in pressure and pulse wave velocity (PWV). PWV is the rate of propagation of the pressure pulse through the arteries, and it depends on the geometry of the vessels and the distensibility of their walls [4]. Although the absolute PWV is partially a function of the dimensions of the vessel, changes in PWV are due principally to alterations in arterial pressure [5]. The relation between mean arterial pressure and changes in PWV has been tested over a wide range of subjects, and is thought to be sufficiently precise and reliable for use in psychophysiology [3,6]. In biofeedback experiments, PWV has several advantages over existing cuff techniques, principally because it allows analogue feedback on every cardiac cycle. Another advantage is that monitoring can be continued for extended periods, removing the necessities for short trials and discontinuous recordings which are intrinsic to occlusion techniques. In this experiment, trials continued for 4 min, and assessment of within as well as between trial modifications was undertaken. An important requirement in studies of learned control is to distinguish the changes in pressure due to feedback from those occurring independently of contingencies as a function of adaptation or immobility in the laboratory. Assessment of the latter has been attempted by employing no-feedback and random feedback control groups, or by monitoring BP before and after feedback training [ 1, 7, 81. In the present study, PWV measurement was continued during the intervals between trials. Analysis of baselines as well as feedback trials could thus be made, and the contribution of the former to the overall results assessed. A number of investigators have recently concluded that analysis of feedback effects from the pre-trial level, rather than the initial baseline, is more appropriate [9, lo]. The effect of repeated sessions was also examined, since training with normotensive groups has commonly been restricted to one or two sessions of less than 1 hr [l, 81. The value of single-session studies of heart rate control has recently been questioned, since adaptation to laboratory conditions may lead to substantial alterations in cardiovascular activity [9]. Additionally, there was some indication in a previous study that BP control became more specific as training progressed [lo]. METHOD
Subjects
The 10 subjects taking part in this study were volunteers with an age range of 19-26 yr, and with no known cardiovascular disorders. There were 5 men and 5 women, and each attended the labora*This work was supported by the Medical Research Council, U.K. tDepartment of Psychiatry, University of Oxford, Warneford Hospital, Oxford. 417
418
ANDREWSTEPTOE and DEREK JOHNSTON
tory for 4 training sessions, spread over a fortnight. earned according to their success at BP control.
They were paid a basic wage, plus rewards
Procedure The experiment was carried out in a light and temperature controlled laboratory adjacent to a control room which housed the polygraph (Devices Equipment Ltd.). The subject was seated in an upright canvas chair placed on an aluminium plate; ECG electrodes were attached to the chest over the Vth intercostal space, respiration was monitored by a mercury and rubber strain gauge round the chest, while electromyographic activity was sampled from the right forearm flexor muscle. The right radial pulse was detected by a “Pixie” strain gauge (Endevco Ltd.) set in a Perspex holder held over the wrist with an elastic strap. Subjects were told that the purpose of the experiment was to gain psychological control over BP. They were instructed to keep still and to make no changes in breathing or movement between rest and trial periods, and also to remember what strategies they were employing so that these could be reported after the session. No changes in BP were to be made during inter-trial rests when the feedback was, of course, not available. Rest and trial periods were indicated by red and green lights on a panel beside the feedback monitor. The required response (Increase or Decrease in BP) and its relation to the feedback and reward systems was also explained. Training consisted of 2 Increase and 2 Decrease sessions, presented alternately in a counterbalanced order, so that five subjects began with Increase and five with Decrease. Physiological monitoring was not started until the subject had been sitting in the laboratory for at least 20 min. The sessions were divided into 10 trials separated by 2 min rests; trials I-4 and 6-9 were 4 min feedback trials, while 5 and 10 were 2 min long and without feedback. At the beginning of each training session a 5 min baseline of all variables was recorded, after which the subject was told the direction of pressure change (Increase or Decrease) which was to be produced. INSTRUMENTATION PWV was monitored by detecting the time interval between the peak of the R wave of the ECG and the foot of the systolic upstroke of the radial pulse. This interval, the transit time, includes a delay due to intracardiac events, but this does not appear to disrupt the relation with BP over the normal pressure range [6]. This modification of PWV monitoring has the advantage of requiring a single peripheral transducer only, leading to greater stability than the two transducer method. Fluctuations in the DC component of the radial pulse signal were reduced before amplification by a baseline Drift Suppressor.* General activity was monitored through the metal plate under the experimental chair. Strain gauges were attached on the underside of each quadrant, and were set in a bridge figuration so that movements would be detected.? A PDP-12 computer was employed to record the variables and control the experiment. The time intervals for transit time (TT), and interbeat interval (IBI) were measured by software detection from the raw amplified signals. Respiration was sampled every 125 msec, while samples of EMG and activity were taken every 100 msec, summed over each second, and stored on magnetic tape. Recording took place throughout trials and during the second minute of each rest. Feedback was provided on the computer oscilloscope and the display relayed to the laboratory via closed circuit television. A sample display is outlined in Fig. 1; the length of the horizontal line
xxxxx
FIG. l.-Feedback
display.
*The Baseline Drift Suppressor was specially made by Mr. Les Aylesbury. tThe design for the activity plate was kindly suggested to us by Dr. Paul Obrist.
The control of blood pressure using pulse-wave velocity feedback
419
was determined on each cardiac cycle by the transit time. Since TT is the inverse of PWV, a drop in BP was indicated by an increase in the length of the line, while a shorter line represented a higher pressure. The correct response was determined by the direction of BP change (Increase or Decrease) required during the trials of that session. Whenever the TT fell the correct side of the vertical criterion line, one of the five stars was removed. When all five had been removed by successive correct responses, a unit worth 4 penny was added to the reward counter. During each trial a histogram of TTs was constructed, so that the median could be calculated. This median was displayed at the end of each trial and acted as criterion for the following trial. A trial-by-trial shaping procedure was thus operated. The criterion for the first trial was determined by TTs recorded during the initial baseline. The display sweep was renewed every 30 msec, so that feedback was continuously available without flickering. At the end of each trial the cumulative money counter was also displayed so that subjects knew how much they had earned to date. The screen remained blank throughout rest periods and no feedback trials. ANALYSIS Since the transit time includes a fixed delay due to intracardiac events, it was not transformed into PWV. The results are thus presented in terms of transit time (the inverse of BP), and interbeat interval (the inverse of heart rate). The mean TT and IBI for the last minute of each rest and the four separate minutes of each feedback trial were calculated for all subjects, except for one where the IBIS were not available.* Several analyses were carried out on these data. The mean TT and IBI during the initial baseline of each session were analysed, likewise values during the inter-trial rests, computed as changes from the initial baseline. Trial changes from the initial baseline were calculated and subjected to analysis of variance, as were change scores between each trial and the pre-trial rest. The latter were intended to assess the precise modifications in activity during trials by filtering out baseline adjustments. For the purposes of analysis, the 4 training periods for each subject were collapsed into 2 sessions, each containing one Increase and one Decrease period. Analysis of variance with 4 within-subject factorsSession, Direction condition, Trial and Minute-within-trial was carried out. Inspection of the respiration, records revealed smooth traces with few irregularities. Accordingly, the respiration rate for selected trials and their preceding rests was counted by hand; data from feedback trials 1,2,7 and 8 were thus assessed, and of these 160 separate trials, only 9 proved unscorable. For the remainder, analyses similar to those for the cardiovascular variables were carried out. Mean activity and EMG per second were also available and were similarly analysed. In all cases, the 8 feedback and 2 no feedback trials were treated separately. RESULTS Initial baseline An analysis of the TTs during the initial baseline yielded no significant effects, thus legitimizing the use of change scores from the basal level. Likewise there were no differences in respiration rate, general activity or EMG throughout the initial baseline. However, in the corresponding IBI analysis, the Direction effect approached significance (F = 4.68, df l/8, p < O.l), the value for Increase being 821 msec, 40 msec longer than that for Decrease. This marginal effect implies that changes in IBI from initial baseline should be treated with caution. Feedback trials The analysis of TT changes during feedback trials from the initial baseline yielded a significant Direction effect (F = 6.3, df l/9, p < 0.05), the mean for Increase being + 1.67 msec, while that for Decrease was + 7.26 msec. That both these values are positive indicates a fall in PWV and BP in both conditions, the change being greater for Decrease. The interaction of Direction x Trial was also significant (F = 259. df 7/63. D < 0.05) and can be inspected in Fig. 2: there is a eradual increase of T? in the decrease condition,-with maintenance near t‘he initial level when subjecrs are instructed to raise pressure. The separation on the final feedback trial is over 11 msec. The effect for Direction x Minute-within-trial (F = 8.83, df 3/27, p < 0.001) can be seen in Table 1. It suggests that in the Increase condition, performance improves between the first and subsequent minutes of trials, while there is little alteration in Decrease. The main effect for Trial attained a significant level of probability (F = 2.42, df 7/63, p < 0.05) due to a trend towards longer TTs as the trials progress. No significant differences between control in the 2 sessions were found. *There were some difficulties with the detection of the R waves of the ECG for one subject. This resulted in 75-95 ‘A R wave and TT detection, but only 38-90x recording of IBIS. It was thus decided to omit the latter from analysis.
420
ANDREWSTEPTOEand DEREK JOHNSTON
The equivalent IBI analysis revealed Direction (F = 21.8, df I/S, p < 0.001) and Trial (F = 4.51, df 7/56, p -c 0.001) effects. The mean IBI change for Decrease was + 50.0 msec, and that for Increase was - 21.6 msec; however, this separation may be affected by the initial difference in IBIS between CHANGES FROM
IN TRANSIT INITIAL
TIME
& INTER-BEAT-INTERVAL
BASELINE
I;;
DECREASE
80
u7
x 2
60
.-c 40 ” 20 .E aX 0% : 0 c” 20 40 FIG. 2.-Mean
TABLE
4
scores for Transit time and inter-beat interval during feedback trials, changes from the initial baseline. Values are averaged across both sessions.
I.-MEAN
TRANSIT
TIMES DURING
Direction
Minute
FEEDBACK TRIALS IN MSEC.~HANGESFROM BASELINE
1
2
3
4
2.81
1.17
1.34
1.35
Decrease
7.25
7.42
7.16
7.21
RESTITRIALCHANGE
Direction Effect-Transit
Decrease Direction
Increase Decrease
THE INITIAL
x Minute within Trial
Increase
Increase
assessed as
SCORES
Time and Inter-beat Interval
Transit time
Inter-beat interval
- 3.22
___ - 30.4 -~~~ 9.37
1.38
x Session-Transit
Session 1 ~~~~ - 4.02 2.23
Time
Session 2 ._ - 2.43 0.53
~-
the two conditions. McCanne and Sandman [9] have suggested that a high initial level facilitates heart rate reduction, while subjects accelerating from a low level are similarly advantaged. The mean IBIS for each trial are shown in Fig. 2. These indicate that TT changes are accompanied by modifications in heart rate. Yet the absence of significant F ratios for Direction x Trial (F = 0.67, df 7/56) and
421
The control of blood pressure using pulse-wave velocity feedback BASELINE CHANGES AND
FROM
Condition Y Rest
FIG. 3.-Mean
INlflALBASELlNE
- TRANSITTIME
INTERBEAT INTERVAL
Periods
-
BP HR
C-----o
BP
C---.
“g
Decrease
Increase
scores for Transit time and inter-beat interval during pre-trial rests assessed as changes from the initial baseline. Values are average across both sessions.
Direction x Minute (F = 0.04, df 3/24) suggests that the alterations in heart rate are more immediate than the progressive divergence in TT. Cardiovascular activity during rests was analysed to determine whether the trial scores from the initial baseline accurately reflect feedback related modifications. The Direction x Rest effect (F = 2.59 df 6/54, p < 0.05) manifest in the TT analysis of variance can be examined in Fig. 3. It implies that BP changes over the inter-trial rests with a gradual reduction over time. Additionally the alterations are not identical in the two direction conditions; in the Rests towards the end of sessions, Increase and Decrease are clearly distinguished. The IBI analysis showed an effect for Rest alone (F = 4.20, df 6/48, p < O.Ol), and no interaction with Direction condition. However, the main effect for Direction approached statistical reliability (F = 3.70, df l/S, p < 0.1). The finding that TTs change over the rests suggests that the analysis of trial changes from the initial baseline does not simply represent modifications due to feedback. In the hope of detecting the REST/TRIAL CHANGE
SCORES
-TRANSIT
+
Session x Direction xTrial
60 -
6Sessioil 1
u7 8.740 : m
-
:4 ;
= 20 .c
-
.c 2 ; .-
rn"
.-:!I : ._
.r z czo2 0
;2
-
40-g4-
FIG. 4.-Mean
6
Session 2
-
z
60 -
TIME & INTER-BEAT-INTERVAL
-
r( # \\ f-d' y-1
\ \ . y‘&
fla> 1, ,/ Y
/\I :;;, \' \' \L L
d'
-\ \
d N -
Bp HR
h \s:F'r V\f u DECREASE
'z_", ;,' INCREASE
scores for Transit time and inter-beat interval during feedback trials assessed as rest to trial changes.
422
ANDREWSTEPTOE and DEREK JOHNSTON
precise modifications which occur when feedback is presented, an analysis of pre-trial to trial values was undertaken. The mean Rest/Trial change scores for feedback trials are shown in Fig. 4. For TT, the Direction (F = 81.5, df l/9, p < 0.001) and Direction x Session (F = 18.4, df l/9, p < 0.01) effects were significant and can be inspected in Table 1. The change in Increase is greater than that in Decrease, in contrast to the apparent superiority of the latter in the Fig. 2 analysis. The interaction of Direction condition with Session is due to an apparent deterioration in performance, the difference between Increase and Decrease falling by over 50 % in the second session. The Direction x Minute interaction (F = 10.0, df 3/27, p < 0.001) once again reflects improved performance in Increase from first to subsequent minutes within trials. The IBI analysis yielded a main effect for Direction (F = 455, df l/8, p -C OGOI) which can be seen in Table 1; the Fvalues for Direction x Session and Direction x Minute interactions do not reach reliable levels, so once again m control is not precisely mirrored by alterations in IBI. The respiration. activity and EMG data were analysed in the same way as the cardiovascular variables, but the effects can be summarized using results from the computation of trial scores as changes from the initial baseline. Table 2 shows the important effects from the respiration rate analysis. The TABLE2.-RESPIRATION RATE--TRIALCHANGESFROMFIRSTBASELINE IN RPM DIRECTION 1.23 -0.90
Increase Decrease
Minute Increase Decrease
1 0.30 - 1.15
DIRECTIONX MINUTE 3 2 1.39 1.56 - 0.70 - 1.09
SESSION X DIRECTION
Session 1 Increase Decrease Sesssion 2 Increase Decrease
1 I a28 - 1.65
2 -0.08--- 1.35
0.85 0.30
1.50 0.58
4 1.68 - 0.65
-
X TRIAL
8 - 0.70---~ - 0.70 2.53 - 1.58
9 0.83 0.95
Trial
3.65 - 1.83
Direction effect (F = 3.95, df 3/27, p -c 0.05) reflects faster breathing in the Increase condition. The Direction x Minute interaction (F = 3.95, df 3/27, p .c 0.05) indicates that the within trial improvement in TT control in the Increase condition is associated with modulation of respiration rate, although some change over the minutes of Decrease trials is also apparent. The triple interaction of Direction x Session x Trial attained significance (F = 7.10, df 3/27, p -c O.Ol), since there is a progressive divergence in breathing rates over the trials of Session 2. These adjustments are not intimately associated with BP control, since there is some indication that TT modifications are reduced in the second session. The analysis of data from the activity plate yielded a Direction effect (F = 7.34, df l/9, p < 0.05); there was a substantial reduction in Decrease while activity remained near the original level in Increase. The Direction x Trial interaction, although significant (F = 3.05, df 7/63, p -e 0.01) does not reflect progressive modifications in activity over trials but a certain amount of fluctuation between them. Analysis of the EMG data yielded no effects approaching significance, and will not be discussed here. No feedback trials
Separate analyses of the rest/trial change scores for TT and IBI during the No Feedback trials were also undertaken. The discrimination between Increase and Decrease was maintained both for TT (F = 18.2, df l/9, p < 0.001) and IBI (F = 20.0, df l/S, p < OWI), while in the former the Direction x Minute interaction was again significant (F = 15.9, df l/9, p < 0.01). Means for these effects can be inspected in Table 3. The data from these trials indicates that modifications in TT are maintained when exteroceptive feedback is withdrawn, and that they are accompanied by HR changes.
The control of blood pressure using pulsewave
TABLE3.-R/T
CHANGE SCORES-NO
FEEDBACK
velocity feedback
TRIALS-~
AND
423
IBI IN MSEC
DIRECTION
TT
Increase Decrease DIREWON
X
IBI
- 2.34
- 24.0
1.94
18.6
MINUTES
(TRANSIT
1 Increase Decrease
-_
TIIvL%)
2
- 1.32
- 3.36
1.67
2.22
DISCUSSION
The results of this study suggest that PWV can be modified with feedback and instructions to alter BP. There are also adjustments in HR, respiration rate and general activity, although the behaviour of these variables indicates only a gross association with the BP modifications. Thus they exhibit no progressive alterations mirroring the gradual divergence in TT seen in Fig. 2. The changes in heart rate imply a pattern of response similar to that seen in the learned control of diastolic pressure, although a recent study of systolic control shows that this too covaries with rate [7, 81. Performance is maintained when feedback is not present, although it should be noted that the no-feedback transfer time was brief. The problem of what measures should be used is clearly exposed in this study. The changes from initial baseline show a pattern of responses similar to that found by other investigators [l, 71; namely that subjects in Decrease exhibit a gradual reduction while those trying to raise pressure maintain it near the baseline. However, the use of this analysis as a reflection of feedback modifications is confounded if changes in baseline occur, and in the present study this is the case. On the other hand, assessment of effects from the level actually present at the onset of trials, as in the rest/trial scores, is incomplete if changes in the running baseline interact with experimental contingencies. McCanne and Sandman [9], recommending analysis from the pre-trial level in studies of heart rate control, did not assess the possibility of differential baseline changes. In a previous study of BP control, Steptoe and Johnston [lo] analyzed trial results as changes from the pre-trial level, and found that modifications with feedback were no greater than those produced on instruction alone. However, since changes in the running baseline were not determined it is uncertain whether such an analysis took account of all the effects of feedback. In the present experiment, the rest/trial data prompt the conclusion that modifications are greater in the Increase than Decrease condition. This type of analysis also reveals a deterioration in performance in the second half of training, which is not reflected by any differential effects in the baseline. The explanation for this is not clear; one possibility is that the Session effect found in the rest/trial analysis is diluted by definite but insignificant differences in the running baseline between the two sessions, so that it does not appear when trials are assessed from the initial level. If the decline in control is a genuine effect, it may be related to the boredom that several subjects reported in the later stages of the experiment.
424
ANDREW STEPTOEand DEREK JOHNSTON
The precise size of changes by individuals in terms of mercury pressure cannot be determined, owing to variation between subjects in the slope of relationship between PWV and BP. However, other data suggest that, on average, a 1 msec change in TT represents a pressure modification of 1 mm Hg [6]. Taking this value, the mean difference between Increase and Decrease in the last trial, using TT changes from the start, is over 11 mm Hg. Future work on the control of BP should recognize that the type of analysis carried out may affect the results obtained. In the light of the finding that baselines shift differentially according to direction of conditions it is difficult to determine the most appropriate method. However, a flexible measurement technique such as PWV monitoring can accommodate the assessment of BP control in a number of different ways. SUMMARY
Ten volunteer subjects each attended four training sessions of 1 hr, during which they were instructed to raise or lower blood pressure. They were provided with immediate analogue feedback of pulse wave velocity from a PDP-12 computer, and successful performance was rewarded with money. Significant differences in PWV between Increase and Decrease conditions were produced, the mean divergence in the final trial being equivalent to 11 mm Hg. These changes were accompanied by adjustments in heart rate and respiration rate, and did not improve with repeated sessionsindeed on some measures deterioration in performance was observed. Neither analysis from the initial baseline nor from the pre-trial level, appears to reflect the precise effects of feedback. Different methods of assessment are discussed, together with the use of PWV as a measure of blood pressure in such experiments. REFERENCES 1. SHAPIROD., SCHWARTZ, G. E. and TURSKY B. Control of blood pressure in man by operant conditioning. Circulation Res. 27, Suppl. 1, 27 (1970). 2. TURSKY B. The indirect recording of human blood pressure. In CardiovascuIar Psychophysiology (OBRIST, P., BLACK A., BRENERJ. and DICARA L. Eds.) Aldine Atherton, Chicago (1974). 3. GRIFIBINB., STEPTOEA. and SLEIGHTP. Pulse Wave velocity as a measure of blood pressure change. Psychophysiology 13, 86 (1976). 4. BERGEL D. H. Properties of blood vessels. In Biochemanics: Its foundations and objectives (FUNG Y., PERRONEN. and ANLIKER M Eds.) Prentice-Hall, Englewood Cliffs, N.J. (1972). 5. BRAMWELLJ. C. and HILL A. V. The velocity of the pulse wave in man. Proc. Roy. Sot. 93, 298 (1922). 6. STEPTOEA., SMULYAN H. and GRIBBON B. Pulse wave velocity and blood pressure change: Calibration and applications (in press). 7. FEY, S. G. and LINDHOLME. Systolic blood pressure and heart rate change during three sessions involving biofeedback or no feedback. Psychophysiology 12, 513 (1975). 8. BRENERJ. Factors influencing the specificity of voluntary cardiovascular control. In Limbic and Autonomic Nervous Systems Research. (DICARA L. Ed) Plenum Press, New York (1974). 9. MCCANNE T. R. and SANDMANC. Determinants of human operant heart rate conditioning. J. Comp. Physiol. Psychol. 88, 609, (1975). 10. STEPTOEA. and JOHNSTOND. The control of blood pressure with instructions and pulse wave velocity feedback. Eur. J. Behav. Anal. Modi’. (in press).
THE CONTROL OF BLOOD PRESSURE USING PULSE-WAVE VELOCITY FEEDBACK* ANDREW
STEPTOE AND
(Received
DEREK
2 January
JOHNSTON~’
1976)
SEVERAL studies of blood pressure (BP) control have recently been carried out using feedback from automated occlusion cuff measurement systems [I, 21. An alternative method for monitoring pressure is based on the relationship between changes in pressure and pulse wave velocity (PWV). PWV is the rate of propagation of the pressure pulse through the arteries, and it depends on the geometry of the vessels and the distensibility of their walls [4]. Although the absolute PWV is partially a function of the dimensions of the vessel, changes in PWV are due principally to alterations in arterial pressure [5]. The relation between mean arterial pressure and changes in PWV has been tested over a wide range of subjects, and is thought to be sufficiently precise and reliable for use in psychophysiology [3,6]. In biofeedback experiments, PWV has several advantages over existing cuff techniques, principally because it allows analogue feedback on every cardiac cycle. Another advantage is that monitoring can be continued for extended periods, removing the necessities for short trials and discontinuous recordings which are intrinsic to occlusion techniques. In this experiment, trials continued for 4 min, and assessment of within as well as between trial modifications was undertaken. An important requirement in studies of learned control is to distinguish the changes in pressure due to feedback from those occurring independently of contingencies as a function of adaptation or immobility in the laboratory. Assessment of the latter has been attempted by employing no-feedback and random feedback control groups, or by monitoring BP before and after feedback training [ 1, 7, 81. In the present study, PWV measurement was continued during the intervals between trials. Analysis of baselines as well as feedback trials could thus be made, and the contribution of the former to the overall results assessed. A number of investigators have recently concluded that analysis of feedback effects from the pre-trial level, rather than the initial baseline, is more appropriate [9, lo]. The effect of repeated sessions was also examined, since training with normotensive groups has commonly been restricted to one or two sessions of less than 1 hr [l, 81. The value of single-session studies of heart rate control has recently been questioned, since adaptation to laboratory conditions may lead to substantial alterations in cardiovascular activity [9]. Additionally, there was some indication in a previous study that BP control became more specific as training progressed [lo]. METHOD
Subjects
The 10 subjects taking part in this study were volunteers with an age range of 19-26 yr, and with no known cardiovascular disorders. There were 5 men and 5 women, and each attended the labora*This work was supported by the Medical Research Council, U.K. tDepartment of Psychiatry, University of Oxford, Warneford Hospital, Oxford. 417
418
ANDREWSTEPTOE and DEREK JOHNSTON
tory for 4 training sessions, spread over a fortnight. earned according to their success at BP control.
They were paid a basic wage, plus rewards
Procedure The experiment was carried out in a light and temperature controlled laboratory adjacent to a control room which housed the polygraph (Devices Equipment Ltd.). The subject was seated in an upright canvas chair placed on an aluminium plate; ECG electrodes were attached to the chest over the Vth intercostal space, respiration was monitored by a mercury and rubber strain gauge round the chest, while electromyographic activity was sampled from the right forearm flexor muscle. The right radial pulse was detected by a “Pixie” strain gauge (Endevco Ltd.) set in a Perspex holder held over the wrist with an elastic strap. Subjects were told that the purpose of the experiment was to gain psychological control over BP. They were instructed to keep still and to make no changes in breathing or movement between rest and trial periods, and also to remember what strategies they were employing so that these could be reported after the session. No changes in BP were to be made during inter-trial rests when the feedback was, of course, not available. Rest and trial periods were indicated by red and green lights on a panel beside the feedback monitor. The required response (Increase or Decrease in BP) and its relation to the feedback and reward systems was also explained. Training consisted of 2 Increase and 2 Decrease sessions, presented alternately in a counterbalanced order, so that five subjects began with Increase and five with Decrease. Physiological monitoring was not started until the subject had been sitting in the laboratory for at least 20 min. The sessions were divided into 10 trials separated by 2 min rests; trials I-4 and 6-9 were 4 min feedback trials, while 5 and 10 were 2 min long and without feedback. At the beginning of each training session a 5 min baseline of all variables was recorded, after which the subject was told the direction of pressure change (Increase or Decrease) which was to be produced. INSTRUMENTATION PWV was monitored by detecting the time interval between the peak of the R wave of the ECG and the foot of the systolic upstroke of the radial pulse. This interval, the transit time, includes a delay due to intracardiac events, but this does not appear to disrupt the relation with BP over the normal pressure range [6]. This modification of PWV monitoring has the advantage of requiring a single peripheral transducer only, leading to greater stability than the two transducer method. Fluctuations in the DC component of the radial pulse signal were reduced before amplification by a baseline Drift Suppressor.* General activity was monitored through the metal plate under the experimental chair. Strain gauges were attached on the underside of each quadrant, and were set in a bridge figuration so that movements would be detected.? A PDP-12 computer was employed to record the variables and control the experiment. The time intervals for transit time (TT), and interbeat interval (IBI) were measured by software detection from the raw amplified signals. Respiration was sampled every 125 msec, while samples of EMG and activity were taken every 100 msec, summed over each second, and stored on magnetic tape. Recording took place throughout trials and during the second minute of each rest. Feedback was provided on the computer oscilloscope and the display relayed to the laboratory via closed circuit television. A sample display is outlined in Fig. 1; the length of the horizontal line
xxxxx
FIG. l.-Feedback
display.
*The Baseline Drift Suppressor was specially made by Mr. Les Aylesbury. tThe design for the activity plate was kindly suggested to us by Dr. Paul Obrist.
The control of blood pressure using pulse-wave velocity feedback
419
was determined on each cardiac cycle by the transit time. Since TT is the inverse of PWV, a drop in BP was indicated by an increase in the length of the line, while a shorter line represented a higher pressure. The correct response was determined by the direction of BP change (Increase or Decrease) required during the trials of that session. Whenever the TT fell the correct side of the vertical criterion line, one of the five stars was removed. When all five had been removed by successive correct responses, a unit worth 4 penny was added to the reward counter. During each trial a histogram of TTs was constructed, so that the median could be calculated. This median was displayed at the end of each trial and acted as criterion for the following trial. A trial-by-trial shaping procedure was thus operated. The criterion for the first trial was determined by TTs recorded during the initial baseline. The display sweep was renewed every 30 msec, so that feedback was continuously available without flickering. At the end of each trial the cumulative money counter was also displayed so that subjects knew how much they had earned to date. The screen remained blank throughout rest periods and no feedback trials. ANALYSIS Since the transit time includes a fixed delay due to intracardiac events, it was not transformed into PWV. The results are thus presented in terms of transit time (the inverse of BP), and interbeat interval (the inverse of heart rate). The mean TT and IBI for the last minute of each rest and the four separate minutes of each feedback trial were calculated for all subjects, except for one where the IBIS were not available.* Several analyses were carried out on these data. The mean TT and IBI during the initial baseline of each session were analysed, likewise values during the inter-trial rests, computed as changes from the initial baseline. Trial changes from the initial baseline were calculated and subjected to analysis of variance, as were change scores between each trial and the pre-trial rest. The latter were intended to assess the precise modifications in activity during trials by filtering out baseline adjustments. For the purposes of analysis, the 4 training periods for each subject were collapsed into 2 sessions, each containing one Increase and one Decrease period. Analysis of variance with 4 within-subject factorsSession, Direction condition, Trial and Minute-within-trial was carried out. Inspection of the respiration, records revealed smooth traces with few irregularities. Accordingly, the respiration rate for selected trials and their preceding rests was counted by hand; data from feedback trials 1,2,7 and 8 were thus assessed, and of these 160 separate trials, only 9 proved unscorable. For the remainder, analyses similar to those for the cardiovascular variables were carried out. Mean activity and EMG per second were also available and were similarly analysed. In all cases, the 8 feedback and 2 no feedback trials were treated separately. RESULTS Initial baseline An analysis of the TTs during the initial baseline yielded no significant effects, thus legitimizing the use of change scores from the basal level. Likewise there were no differences in respiration rate, general activity or EMG throughout the initial baseline. However, in the corresponding IBI analysis, the Direction effect approached significance (F = 4.68, df l/8, p < O.l), the value for Increase being 821 msec, 40 msec longer than that for Decrease. This marginal effect implies that changes in IBI from initial baseline should be treated with caution. Feedback trials The analysis of TT changes during feedback trials from the initial baseline yielded a significant Direction effect (F = 6.3, df l/9, p < 0.05), the mean for Increase being + 1.67 msec, while that for Decrease was + 7.26 msec. That both these values are positive indicates a fall in PWV and BP in both conditions, the change being greater for Decrease. The interaction of Direction x Trial was also significant (F = 259. df 7/63. D < 0.05) and can be inspected in Fig. 2: there is a eradual increase of T? in the decrease condition,-with maintenance near t‘he initial level when subjecrs are instructed to raise pressure. The separation on the final feedback trial is over 11 msec. The effect for Direction x Minute-within-trial (F = 8.83, df 3/27, p < 0.001) can be seen in Table 1. It suggests that in the Increase condition, performance improves between the first and subsequent minutes of trials, while there is little alteration in Decrease. The main effect for Trial attained a significant level of probability (F = 2.42, df 7/63, p < 0.05) due to a trend towards longer TTs as the trials progress. No significant differences between control in the 2 sessions were found. *There were some difficulties with the detection of the R waves of the ECG for one subject. This resulted in 75-95 ‘A R wave and TT detection, but only 38-90x recording of IBIS. It was thus decided to omit the latter from analysis.
420
ANDREWSTEPTOEand DEREK JOHNSTON
The equivalent IBI analysis revealed Direction (F = 21.8, df I/S, p < 0.001) and Trial (F = 4.51, df 7/56, p -c 0.001) effects. The mean IBI change for Decrease was + 50.0 msec, and that for Increase was - 21.6 msec; however, this separation may be affected by the initial difference in IBIS between CHANGES FROM
IN TRANSIT INITIAL
TIME
& INTER-BEAT-INTERVAL
BASELINE
I;;
DECREASE
80
u7
x 2
60
.-c 40 ” 20 .E aX 0% : 0 c” 20 40 FIG. 2.-Mean
TABLE
4
scores for Transit time and inter-beat interval during feedback trials, changes from the initial baseline. Values are averaged across both sessions.
I.-MEAN
TRANSIT
TIMES DURING
Direction
Minute
FEEDBACK TRIALS IN MSEC.~HANGESFROM BASELINE
1
2
3
4
2.81
1.17
1.34
1.35
Decrease
7.25
7.42
7.16
7.21
RESTITRIALCHANGE
Direction Effect-Transit
Decrease Direction
Increase Decrease
THE INITIAL
x Minute within Trial
Increase
Increase
assessed as
SCORES
Time and Inter-beat Interval
Transit time
Inter-beat interval
- 3.22
___ - 30.4 -~~~ 9.37
1.38
x Session-Transit
Session 1 ~~~~ - 4.02 2.23
Time
Session 2 ._ - 2.43 0.53
~-
the two conditions. McCanne and Sandman [9] have suggested that a high initial level facilitates heart rate reduction, while subjects accelerating from a low level are similarly advantaged. The mean IBIS for each trial are shown in Fig. 2. These indicate that TT changes are accompanied by modifications in heart rate. Yet the absence of significant F ratios for Direction x Trial (F = 0.67, df 7/56) and
421
The control of blood pressure using pulse-wave velocity feedback BASELINE CHANGES AND
FROM
Condition Y Rest
FIG. 3.-Mean
INlflALBASELlNE
- TRANSITTIME
INTERBEAT INTERVAL
Periods
-
BP HR
C-----o
BP
C---.
“g
Decrease
Increase
scores for Transit time and inter-beat interval during pre-trial rests assessed as changes from the initial baseline. Values are average across both sessions.
Direction x Minute (F = 0.04, df 3/24) suggests that the alterations in heart rate are more immediate than the progressive divergence in TT. Cardiovascular activity during rests was analysed to determine whether the trial scores from the initial baseline accurately reflect feedback related modifications. The Direction x Rest effect (F = 2.59 df 6/54, p < 0.05) manifest in the TT analysis of variance can be examined in Fig. 3. It implies that BP changes over the inter-trial rests with a gradual reduction over time. Additionally the alterations are not identical in the two direction conditions; in the Rests towards the end of sessions, Increase and Decrease are clearly distinguished. The IBI analysis showed an effect for Rest alone (F = 4.20, df 6/48, p < O.Ol), and no interaction with Direction condition. However, the main effect for Direction approached statistical reliability (F = 3.70, df l/S, p < 0.1). The finding that TTs change over the rests suggests that the analysis of trial changes from the initial baseline does not simply represent modifications due to feedback. In the hope of detecting the REST/TRIAL CHANGE
SCORES
-TRANSIT
+
Session x Direction xTrial
60 -
6Sessioil 1
u7 8.740 : m
-
:4 ;
= 20 .c
-
.c 2 ; .-
rn"
.-:!I : ._
.r z czo2 0
;2
-
40-g4-
FIG. 4.-Mean
6
Session 2
-
z
60 -
TIME & INTER-BEAT-INTERVAL
-
r( # \\ f-d' y-1
\ \ . y‘&
fla> 1, ,/ Y
/\I :;;, \' \' \L L
d'
-\ \
d N -
Bp HR
h \s:F'r V\f u DECREASE
'z_", ;,' INCREASE
scores for Transit time and inter-beat interval during feedback trials assessed as rest to trial changes.
422
ANDREWSTEPTOE and DEREK JOHNSTON
precise modifications which occur when feedback is presented, an analysis of pre-trial to trial values was undertaken. The mean Rest/Trial change scores for feedback trials are shown in Fig. 4. For TT, the Direction (F = 81.5, df l/9, p < 0.001) and Direction x Session (F = 18.4, df l/9, p < 0.01) effects were significant and can be inspected in Table 1. The change in Increase is greater than that in Decrease, in contrast to the apparent superiority of the latter in the Fig. 2 analysis. The interaction of Direction condition with Session is due to an apparent deterioration in performance, the difference between Increase and Decrease falling by over 50 % in the second session. The Direction x Minute interaction (F = 10.0, df 3/27, p < 0.001) once again reflects improved performance in Increase from first to subsequent minutes within trials. The IBI analysis yielded a main effect for Direction (F = 455, df l/8, p -C OGOI) which can be seen in Table 1; the Fvalues for Direction x Session and Direction x Minute interactions do not reach reliable levels, so once again m control is not precisely mirrored by alterations in IBI. The respiration. activity and EMG data were analysed in the same way as the cardiovascular variables, but the effects can be summarized using results from the computation of trial scores as changes from the initial baseline. Table 2 shows the important effects from the respiration rate analysis. The TABLE2.-RESPIRATION RATE--TRIALCHANGESFROMFIRSTBASELINE IN RPM DIRECTION 1.23 -0.90
Increase Decrease
Minute Increase Decrease
1 0.30 - 1.15
DIRECTIONX MINUTE 3 2 1.39 1.56 - 0.70 - 1.09
SESSION X DIRECTION
Session 1 Increase Decrease Sesssion 2 Increase Decrease
1 I a28 - 1.65
2 -0.08--- 1.35
0.85 0.30
1.50 0.58
4 1.68 - 0.65
-
X TRIAL
8 - 0.70---~ - 0.70 2.53 - 1.58
9 0.83 0.95
Trial
3.65 - 1.83
Direction effect (F = 3.95, df 3/27, p -c 0.05) reflects faster breathing in the Increase condition. The Direction x Minute interaction (F = 3.95, df 3/27, p .c 0.05) indicates that the within trial improvement in TT control in the Increase condition is associated with modulation of respiration rate, although some change over the minutes of Decrease trials is also apparent. The triple interaction of Direction x Session x Trial attained significance (F = 7.10, df 3/27, p -c O.Ol), since there is a progressive divergence in breathing rates over the trials of Session 2. These adjustments are not intimately associated with BP control, since there is some indication that TT modifications are reduced in the second session. The analysis of data from the activity plate yielded a Direction effect (F = 7.34, df l/9, p < 0.05); there was a substantial reduction in Decrease while activity remained near the original level in Increase. The Direction x Trial interaction, although significant (F = 3.05, df 7/63, p -e 0.01) does not reflect progressive modifications in activity over trials but a certain amount of fluctuation between them. Analysis of the EMG data yielded no effects approaching significance, and will not be discussed here. No feedback trials
Separate analyses of the rest/trial change scores for TT and IBI during the No Feedback trials were also undertaken. The discrimination between Increase and Decrease was maintained both for TT (F = 18.2, df l/9, p < 0.001) and IBI (F = 20.0, df l/S, p < OWI), while in the former the Direction x Minute interaction was again significant (F = 15.9, df l/9, p < 0.01). Means for these effects can be inspected in Table 3. The data from these trials indicates that modifications in TT are maintained when exteroceptive feedback is withdrawn, and that they are accompanied by HR changes.
The control of blood pressure using pulsewave
TABLE3.-R/T
CHANGE SCORES-NO
FEEDBACK
velocity feedback
TRIALS-~
AND
423
IBI IN MSEC
DIRECTION
TT
Increase Decrease DIREWON
X
IBI
- 2.34
- 24.0
1.94
18.6
MINUTES
(TRANSIT
1 Increase Decrease
-_
TIIvL%)
2
- 1.32
- 3.36
1.67
2.22
DISCUSSION
The results of this study suggest that PWV can be modified with feedback and instructions to alter BP. There are also adjustments in HR, respiration rate and general activity, although the behaviour of these variables indicates only a gross association with the BP modifications. Thus they exhibit no progressive alterations mirroring the gradual divergence in TT seen in Fig. 2. The changes in heart rate imply a pattern of response similar to that seen in the learned control of diastolic pressure, although a recent study of systolic control shows that this too covaries with rate [7, 81. Performance is maintained when feedback is not present, although it should be noted that the no-feedback transfer time was brief. The problem of what measures should be used is clearly exposed in this study. The changes from initial baseline show a pattern of responses similar to that found by other investigators [l, 71; namely that subjects in Decrease exhibit a gradual reduction while those trying to raise pressure maintain it near the baseline. However, the use of this analysis as a reflection of feedback modifications is confounded if changes in baseline occur, and in the present study this is the case. On the other hand, assessment of effects from the level actually present at the onset of trials, as in the rest/trial scores, is incomplete if changes in the running baseline interact with experimental contingencies. McCanne and Sandman [9], recommending analysis from the pre-trial level in studies of heart rate control, did not assess the possibility of differential baseline changes. In a previous study of BP control, Steptoe and Johnston [lo] analyzed trial results as changes from the pre-trial level, and found that modifications with feedback were no greater than those produced on instruction alone. However, since changes in the running baseline were not determined it is uncertain whether such an analysis took account of all the effects of feedback. In the present experiment, the rest/trial data prompt the conclusion that modifications are greater in the Increase than Decrease condition. This type of analysis also reveals a deterioration in performance in the second half of training, which is not reflected by any differential effects in the baseline. The explanation for this is not clear; one possibility is that the Session effect found in the rest/trial analysis is diluted by definite but insignificant differences in the running baseline between the two sessions, so that it does not appear when trials are assessed from the initial level. If the decline in control is a genuine effect, it may be related to the boredom that several subjects reported in the later stages of the experiment.
424
ANDREW STEPTOEand DEREK JOHNSTON
The precise size of changes by individuals in terms of mercury pressure cannot be determined, owing to variation between subjects in the slope of relationship between PWV and BP. However, other data suggest that, on average, a 1 msec change in TT represents a pressure modification of 1 mm Hg [6]. Taking this value, the mean difference between Increase and Decrease in the last trial, using TT changes from the start, is over 11 mm Hg. Future work on the control of BP should recognize that the type of analysis carried out may affect the results obtained. In the light of the finding that baselines shift differentially according to direction of conditions it is difficult to determine the most appropriate method. However, a flexible measurement technique such as PWV monitoring can accommodate the assessment of BP control in a number of different ways. SUMMARY
Ten volunteer subjects each attended four training sessions of 1 hr, during which they were instructed to raise or lower blood pressure. They were provided with immediate analogue feedback of pulse wave velocity from a PDP-12 computer, and successful performance was rewarded with money. Significant differences in PWV between Increase and Decrease conditions were produced, the mean divergence in the final trial being equivalent to 11 mm Hg. These changes were accompanied by adjustments in heart rate and respiration rate, and did not improve with repeated sessionsindeed on some measures deterioration in performance was observed. Neither analysis from the initial baseline nor from the pre-trial level, appears to reflect the precise effects of feedback. Different methods of assessment are discussed, together with the use of PWV as a measure of blood pressure in such experiments. REFERENCES 1. SHAPIROD., SCHWARTZ, G. E. and TURSKY B. Control of blood pressure in man by operant conditioning. Circulation Res. 27, Suppl. 1, 27 (1970). 2. TURSKY B. The indirect recording of human blood pressure. In CardiovascuIar Psychophysiology (OBRIST, P., BLACK A., BRENERJ. and DICARA L. Eds.) Aldine Atherton, Chicago (1974). 3. GRIFIBINB., STEPTOEA. and SLEIGHTP. Pulse Wave velocity as a measure of blood pressure change. Psychophysiology 13, 86 (1976). 4. BERGEL D. H. Properties of blood vessels. In Biochemanics: Its foundations and objectives (FUNG Y., PERRONEN. and ANLIKER M Eds.) Prentice-Hall, Englewood Cliffs, N.J. (1972). 5. BRAMWELLJ. C. and HILL A. V. The velocity of the pulse wave in man. Proc. Roy. Sot. 93, 298 (1922). 6. STEPTOEA., SMULYAN H. and GRIBBON B. Pulse wave velocity and blood pressure change: Calibration and applications (in press). 7. FEY, S. G. and LINDHOLME. Systolic blood pressure and heart rate change during three sessions involving biofeedback or no feedback. Psychophysiology 12, 513 (1975). 8. BRENERJ. Factors influencing the specificity of voluntary cardiovascular control. In Limbic and Autonomic Nervous Systems Research. (DICARA L. Ed) Plenum Press, New York (1974). 9. MCCANNE T. R. and SANDMANC. Determinants of human operant heart rate conditioning. J. Comp. Physiol. Psychol. 88, 609, (1975). 10. STEPTOEA. and JOHNSTOND. The control of blood pressure with instructions and pulse wave velocity feedback. Eur. J. Behav. Anal. Modi’. (in press).