Non invasive continuous arterial pressur

Research Paper

Clinical Autonomic Research 7, 97-101 (1997)

The haemodynamic effects of head-up tilt (HUT) at different
tilt angles were investigated non-invasively in eight normal male
subjects. Mean arterial pressure (MAP; by Ohmeda Finapres
2300), stroke volume (SV) and heart rate (HR; by BoMed
NCCOM3-R7S) were continuously recorded whilst performing
a series of HUTs (55 ~ 10~ 20 ~ 30 ~ and 55 ~ lasting 3 min
each. The response to HUT was proportional to the sine of the
tilt angle. The magnitude of the response varied between subjects. HUT to 55 ~ resulted in mean (95% confidence limits)
increases in MAP by 16 (+ 16)% and HR by 11 (• 24)% and a
decrease in SV by -25 (+ 22)%. These results were repeatable
after 30 min. At small tilt angles, i.e. g 20 ~ MAP did not
change and HR decreased by -3 (+ 4)%. A detailed analysis
revealed immediate dynamic (0-30 s), late dynamic (30-90 s)
and plateau (after 90 s) phases in the response to HUT. In conclusion, HUT produces reproducible haemodynamic effects,
although differences exist among subjects. A detailed analysis of
these effects can be successfully performed using non-invasive
methods.


Non-invasive continuous
arterial pressure, heart rate
and stroke volume measurements during graded head-up
tilt in normal man

Keywords: tilting; postural stress; monitoring; non-invasive; blood
pressure; cardiac output; impedance cardiography; Finapres

Correspondence and reprint requests: Dr Lester A.H. Critchley,
Department of Anaesthesia & Intensive Care, The Chinese University
ofHong Kong, Prince of Wales Hospital, Shatin, Hong Kong.
Tel: (+852) 2632 2735; Fax: (+852) 2637 2422; e-mail: hcritchley@cuhk.edu.hk

L.A.H. Critchley MD FFARCSI 1, F. Conway MB BCh
P.J. Anderson RN MPhil 2, B. Tomlinson
MD FRCP 2 and J.A.J.H. Critchley PhD FRCP 2
Departments of 1Anaesthesia & Intensive Care and
2Clinical Pharmacology, The Chinese University of Hong
Kong, Prince of Wales Hospital, Shatin, Hong Kong

FFARCSl 1,

Received9 September1996" acceptedin revbedform 6January 1997

Introduction

Head-up tilting is an accepted method of producing a
reproducible haemodynamic challenge to the cardiovascular system. It is commonly used by clinical pharmacologists in cardiovascular drug research, as well as
being a diagnostic tool for investigating autonomic
dysfunction 1 and for describing the pathophysiology
of various medical conditions. Head-up tilt creates a
postural or gravitational challenge to the cardiovascular system due to a reduction in venous blood return
and hence the venous filling of the heart with a consequent decrease in stroke volume (SV). This leads to a
reduction in arterial pressure, which via the arterial
baroreceptors results in a c o m p e n s a t o r y cardioacceleratory response (increase in heart rate; HR) and
vasopressor response (i.e. increase in peripheral resistance).2
Until recently, these haemodynamic effects could
only be measured intermittently. However, with the
development of continuous non-invasive monitoring
techniques and improved data acquisition systems, a

more detailed analysis of head-up tilt can now be performed. In this article we describe a data collection
system which employs non-invasive arterial pressure
m e a s u r e m e n t using the O h m e d a 2300 Finapres
(Ohmeda, Englewood, CO, USA) and non-invasive
SV and cardiac output measurement using the BoMed
NCCOM3-RTS (BoMed Ltd, Irvine, CA, USA). We
used this system to investigate the immediate and

intermediary effects of head-up tilt, using a series of
tilt angles, in eight healthy male volunteers.
Materials and methods

The study was approved by the local Clinical Research
Ethics Committee of the Chinese University of Hong
Kong. We recruited eight healthy adult male volunteers from within our departments. All subjects were
studied in the mid-afternoon and were at least 2 h
post prandial. Tilting was performed manually using
an Akron 8632 tilt table (Akron Therapy Products
Ltd, Ipswich, UK).
Following arrival in the laboratory, the subject

assumed a supine-horizontal position on the tilt table.
The BoMed NCCOM3-R7S was attached to the subject using an eight electrode montage) This involved
two pairs of diametrically opposite impedance measuring electrodes placed laterally at the base of the neck and
at the level of the xiphoid sternum. Current injecting
electrodes were placed 5 cm distal to each impedance
measuring electrode. Prior to electrode placement, the
skin was cleaned and degreased with alcohol to improve
electrical contact. The Finapres was wrapped around the
subject's left middle finger and the subject's hand was
kept at a constant level with respect to the heart. An
arterial pressure cuff, which was used for initial calibration of the Finapres, was attached to the left upper arm.
The Finapres (name derived from Finger _arterial pressure) measures arterial pressure (diastolic, mean and sys9 1997 Rapid Science Publishers

97

L.A.H. Critchley et al.

tolic) continuously. The system measures total arterial
blood volume in the finger using an infrared plethysmographic method. A finger cuff is attached to the subject's
middle finger. The pressure of the cuff is modulated by a

servo mechanism which maintains a constant arterial
blood volume within the finger. Arterial pressure is measured directly from the cuff pressure, which is proportional to arterial pressure. The system is calibrated by an
automated oscillotonometer attached to the upper arm.
The finger cuff should be maintained at the level of the
heart to measure arterial pressure accurately.4
The BoMed measures beat-to-beat SV from the
waveform of the impedance changes with the thorax.
These are detected by passing a 70 kHz, 2.5 mA current
through the thorax using paired neck and lower thoracic
electrodes. A second set of paired neck and lower thoracic electrodes measures the thoracic impedance, which
varies cyclically with the cardiac cycle. From the impedance waveform two important variables are measured:
the peak flow in the aorta and the duration of ventricular ejection; these measurements enable SV to be calculated. A calibration factor is also required, which is
derived from a standard formula that treats the thorax as
a truncated cone. The methodology is fully described by
Bernstein. 5 The BoMed was set to record beat-to-beat
readings of cardiac output, SV and HR.
Data from both the Finapres and BoMed were
acquired and stored on a laptop computer (Bondwell
B3105X) as a spread-sheet file (Excel 4.0, Microsoft,
USA) for subsequent analysis.

Following a 10-min rest period to allow the haemodynamic variables to stabilize, the subjects were tilted
head-up five times. The tilt angles used were 55 ~ 10~
20 ~, 30 ~ and 55 ~. The first and last tilts were used to
test the repeatability of the tilting manoeuvre. During
the tilting the subject remained quiet and undisturbed.
Baseline data were collected with the subject supine for
3 min. The subject was then rapidly tilted head-up,
over 1-3 s, to the set tilt angle and kept at this angle for
3 min before being rapidly returned to the horizontal,
where he was kept for 3 min before the next head-up
tilt. Overall data collection lasted 33 min.

the tilting protocol. The magnitudes of the changes in
each variable, expressed as the percentage change from
the pre-tilt baseline, were calculated for each tilt angle
using data from the middle, or steady-state, period of
each tilt (i.e. 60-150 s) for each subject. Percentage
data from each subject were then combined to give
overall percentage changes for each tilt angle. The
repeatability of BoMed stroke volume measurements

taken during the tilting protocol was assessed by comparing steady-state measurements using the method of
Bland and Altman. 6 Measurements taken before and
during the two 55 ~ head-up tilts were compared.
Student's t test, analysis of variance and linear
regression were used for statistical analysis. Results are
presented as means with range or SD. p < 0.05 was
considered significant.

Results
Data from eight healthy male subjects (mean (range)),
age 38 (30-45) years, weight 75 (60-95) kg and
height 173 (160-182) cm are presented. Their baseline (mean (SD)) systolic arterial pressure (SAP) was
118 (17) mmHg, MAP was 82 (16) mmHg, SV was
54 (15) ml, HR was 68 (11) beats/min and derived
SVR was 1911 (542) dyn s cm-5.
The overall haemodynamic effects of the different
angles of tilt are shown in Figure 1. SV decreased and
derived SVR increased at all four angles of tilt. SAP
and MAP increased only after tilting to at least 20 ~.
HR decreased with small angles of tilt (i.e. 10 ~ but

increased with larger angles of tilt (i.e. 55 ~ (all p <
0.0001). The magnitudes of the h a e m o d y n a m i c
t 88 91]
80

70

,

,~'~

t

.

J

i

'


~

.

i

.

1

.

i

i

~

MAP


i

HR

, ju

60
50
48
~2

Analysis and statistics
All haemodynamic data were recorded on an Excel 4.0
spread-sheet file. The beat-to-beat data were averaged
to give readings for each 10-s period of the study
using Excel subroutines 'macros'. The variables used in
the analysis were Finapres mean arterial pressure
(MAP), SV and HR. Systemic vascular resistance
(SVR) was derived from the following formula:

SVR

MAP • 80
-

SV • HR

(dyn s cm-5)

Data from all subjects were averaged for each 10-s
time interval to give the overall trend with time for
98

Clinical A u t o n o m i c R e s e a r c h ~ vol 7 ~ 1 9 9 7

Ig

30

o

ZO

,

i
,

R*
i

i

: 55 ~

', 18 ~

', Z8 O

i

~

i

J

I B

i

20

: 38 ~

: 55 ~

x

X

r

38

Time (min)
Figure 1. Effects of head-up tilting for 3 min, with 3-min rest periods
between tilts, at different tilt angles (55 ~ 10 ~ 20 ~ 30 ~ and 55~ Three
measured variables, mean arterial pressure (MAP), heart rate (HR) and
stroke volume (SV) and the derived systemic vascular resistance (SVR)
are plotted. SVR*, SVR divided by 100 (i.e. SVR/100). A logarithmic scale
was used on the y-axis so that the relative magnitudes of the responses
could be represented. The vertical dotted lines show the times of commencing each head-up tilt

Graded head-up tilt
Table 1. Percentage changes (mean (95% confidence limits ))
from baseline in measured h a e m o d y n a m i c variables at each
angle of tilt (degrees)
Angle of tilt
55 ~
10 ~
20 ~
30 ~
55 ~

% MAP
16
0
7
9
15

% SV

(0 to 32)**
(-6 to 6)
(-1 to 15)**
(-5 to 23)**
(-3 to 33)**

-25
-7
-16
-21
-25

(-47
(-17
(-32
(-41
(-47

188

11 (-13 to 35)**
- 3 (-7 to 1 )**
2 (-6 to 10)
5(-11 to21)
13 (-17 to 30)**

w

85

~
~. 75

'

78

,

i

,

65

up fill

",

4.8
s

3.8

1
68

N

~"
IE

se
i

MAP, Mean arterial pressure; SV, stroke volume; HR, heart rate.
Significant differences c o m p a r e d with the horizontal position
shown as *p < 0.05, **p < 0.01. No significant difference in variables between the initial and final 55 ~ tilts.

changes at each angle of tilt are shown in Table 1. The
magnitudes of these changes were related to the tilt
angle (Figure 2). However, there was a large variation
between individuals in the magnitude of the response
(Table 1).
A more detailed analysis of the MAP, SV and HR
waveforms with tilting showed several definite stages in
the response to head-up tilt (Figure 3). The following
phases could be defined for 55 ~ of tilt. The dynamic
and steady-state phases following head-up tilting were:
(i) a rapid immediate increase in MAP and HR and
decrease in SV lasting about 30 s; (ii) a further slow
increase in MAP and HR and decrease in SV lasting
approximately 1 min; (iii) a steady-state phase for the
remainder of the head-up tilt. Dynamic phases following return to the horizontal position were: (iv) a rapid
immediate decrease in MAP and HR and increase in
SV; (v) a further slow increase in SV and, surprisingly,
MAP,, with a decrease in HR lasting 1-2 min.
The effects of the first and last 55 ~ head-up tilt
were essentially similar (Table 1). Paired SV measure-

E
E

911

% HR

to -3)**
to 3)**
to 0)**
to-l)**
to -3)**

~

95

!

c

3.5
3.2

45
, '

411

35

i

-I

i

8

I

l

I

2

3

L
i

4

Time (min)
Figure 3. Detailed effects of 55~ head-up tilt on mean arterial pressure
(MAP, A), stroke volume (SV, O), cardiac output (CO, ~) and heart rate
(HR, +). The dynamic (immediate (I) and late (L)) and steady-state (S)
phases are shown

18-

.

E

g

.

.

.....

.

.

.

.

.

.

.

.

.

.

.

.

i9

.

.

"t-

9

. . . . . . . . . . . . . . . .

9

28

MAP
--5

_.~

~

18

HR

f13

,~.

-18
28

,E

8

~

. . . . . .

T

?

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.~ -28
n.

SV

8

,

,

I

8.2

8.4

8.6

,
48

5'8

6'8

,

,

78

88

Figure 4. Bland and Altman 6 plot showing comparative stroke volume
readings taken either before or during the first (a) and last (b) 55~ head-up
tilts from eight male subjects. Scales are bias ( S V b - S V a ) in ml and mean
stroke volume ((SV b + SVa)/2 ) in ml. Limits of agreement (p • 2SD) or •
10% are shown

~ -18
na

-38

,
38

,
8.8

Sine of tilt angle
Figure 2. Linear relationship between the mean (SEM) values for mean
arterial pressure (MAP), stroke volume (SV) and heart rate (HR) in eight
subjects and the sine of the tilt angle

ments taken before and during the 55 ~ head-up tilting
were linearly related: SVb = (0.94) SV, + 3.1 (r =
0.99). The Bland and Altman plot 6 showed limits of
agreement (p _+ 2SD) o f - 0 . 1 _+ 4.7 ml (Figure 4).
Mean cardiac output was 47.8 ml giving percentage
limits of + 10%.
There was an inverse correlation between the magnitudes of the changes in SV and HR with an r value
of 0.78 (? < 0.0001). The relationship between the
percentage changes in MAP, SV and HR and the sine
Clinical Autonomic Research 9vol 7 91997

99

L.A.H. Critchley et al.

of the angle tilt is shown in Figure 2. Extrapolation of
percentage changes of variables in Figure 2 predicted
that full head-up tilt (i.e. 90~ without standing,
would have caused an increase in MAP of 20% and
HR of 16% and a decrease in SV of 32%. As cardiac
output = SV • HR, the predicted change in cardiac
output was 16%.
Discussion
Several different protocols for using head-up tilting
are described in the literature. Single head-up tilt to
70-85 ~ has been commonly used. 7"8 This technique
ensures the maximum response without the subject
weight bearing. Standing alters the response to headup tilting because of active factors such as the muscle
pumps in the legs being activated, which increase the
venous return to the heart. Gradual tilt to multiple tilt
angles has also been used) Recently, there has been a
renewed interest in prolonged tilting and in particular
head-down tilting, especially in relation to endocrine
responses and H R variability. The effects of graded (to
a series of angles) head-up tilt have only been studied
previously using intermittent assessments of cardiac
output. 9-11 In the present study we describe these
effects more fully using continuous measurements.
Alternative methods of challenging cardiovascular
reflexes do exist, such as using an exercise bicycle, giving stimulatory i.v. drugs such as isoprenaline and
phenylephrine and the use of negative pressure on the
lower half of the body. However, head-up tilt is the
simplest, probably most reproducible and therefore
most attractive of these techniques, especially when
used in the clinical setting.
The validity of head-up tilt as a test in drug trials
has been questioned by de Mey and Enterling. 12'13
They found that a subject's response could vary significantly from day to day and in particular the ingestion
of food .could affect the results. Several of their subjects showed a variant response to head-up tilt, with
acute decreases in H R and arterial pressure which
were presumably vagal in origin. However, as the present study did not involve repeat studies in the same
subject, variations in response within subjects was not
a problem. However, we were aware of the potential
problems associated with the ingestion of food and
environmental factors. We thus studied all subjects in
the mid afternoon when they were at least 2 h post
prandial.
The standard method of measuring arterial pressures continuously is by an intra-arterial catheter connected to a pressure transducer. The Finapres has been
shown to be a reliable alternative to intra-arterial
monitoring, when following acute changes in arterial
pressure. 4'~4'15 By using the Finapres, we also avoided
the potential dangers and inconvenience of intraarterial monitoring.
It is generally accepted by anaesthetists and clinical
100

Clinical Autonomic Research ~ vol 7 ~ 1997

pharmacologists that impedance cardiac output measurements follow changes in SV and cardiac output
reliably in normal healthy subjects, and this belief is
supported by several successful clinical studies. 16-I9
However, several circumstances are known to impair
the accuracy of impedance cardiac output measurements and these include high and low cardiac output
states, obesity and cardiac anomalies. 2~ The accuracy
of the technique is also significantly impaired in the
critically ill patient and comparisons with thermodilution in these patients result in limits of agreement as
wide as +_ 50-60%31-23 However, validation studies
are hindered because no gold standard method of
measuring cardiac output currently exists clinically.
Thermodilution, which is the current clinical standard, is only accurate to -+ 15-20%. 20 Furthermore,
when trending is assessed, current standards only measure cardiac output intermittently and significant
problems exist when one tries to alter the patient's cardiac output either physically or pharmacologically.
Also, the true value of cardiac output is continually
changing due to normal physiological factors such as
respiration. Hence, as few investigators have managed
to show that the BoMed can trend SV and cardiac
output measurements satisfactorily, TM the findings of
our study are of value because we show that in normal
subjects changes in SV can be measured to an accuracy of at least + 10% over a 30-min period.
According to Blomqvist and Stone, 2 passive headup tilt to a near-upright posture results in a redistribution of venous blood to the deep veins of legs of up to
500 ml, and to the gluteal and pelvic veins of up to
200-300 ml. Although there is a large inter-individual
variation, SV decreases on average by 33%, with an
associated small increase in HR, and cardiac output
decreases by 20% on average. When changing from a
supine to a seated posture, which is similar to head-up
tilt, Coonan and Hope 24 quoted slightly higher figures
than Blomqvist and Stone, with central blood volume
decreasing by 400 ml, arterial pressure increasing by
0-20%, SV decreasing by 40-50% and HR increasing
by 15-30%. From our results we predicted similar
haemodynamic changes to Blomqvist and Stone, 2 with
MAP increasing by 20%, SV decreasing by 32% and
HR increasing by 16%. We also found a similar large
inter-individual variation in the size of the response to
head-up tilting (Table 1).
We found that the percentage changes in variables
were proportional to the sine of the tilt angle (Figure 2).
This relationship was predictable because the gravitation effect of tilting is proportional to the sine of the tilt
angle. At small tilt angies (i.e. 10~ H R decreased
rather than increased, which has not been reported
previously. The most likely explanation is that the HR
initially decreases at small tilt angles, i.e. 10~, because of
the reduced stimulation of volume receptors in the
right atrium and great vessels of the heart, because of
the reduction in venous return. However, at greater

Graded head-up tilt
angles of tilt the baroreceptor reflex becomes activated,
causing increases in HR and arterial pressure.
By using our simple computerized data acquisition
system to collect real-time data from both the Finapres
and the BoMed, we were able to give a more detailed
description of the cardiovascular effects of head-up tilt.
We were also able to define a dynamic or rapid phase,
which had immediate and late components, and a
steady-state phase. However, more long-term effects
(i.e. after 3 min) were not studied. The immediate
dynamic phase lasted approximately 30 s and most
likely represented the redistribution of venous blood to
the lower extremities, with the accompanying decrease
in SV and increases in MAP and HR. The late dynamic
phase lasted approximately 60 s and was less easy to
explain. The late phase may have represented an adaptation of the venous system as it became distended with
venous blood in response to the increased hydrostatic
pressure in the lower extremities. Acute fluid shifts are
also known to occur during posturing; 2 however, the
time period involved makes this explanation unlikely.
These acute phases in the tilt response may prove a
useful tool in evaluating the effects of drugs acting on
the cardiovascular system. However, if steady-state
conditions during tilting are being studied, one needs
to wait at least 90 s before taking measurements, in
order that the dynamic phase is completed. This was
incorporated into the present study when calculating
the magnitudes of each steady-state head-up tilt.
References
1. de Mey C, Enterling D. Assessment of the hemodynamic response
to single passive head-up tilt by non-invasive methods in normotensive subjects. Methods Find Exp Clin Pharmacol 1986; 8: 449-457.
2. Blomqvist CG, Stone HL. Cardiovascular adjustments to gravitational stress. In: American Physiology Society, eds. Handbook of
Physiology: The Cardiovascular System. Baltimore: Williams and
Wilkins, 1983; 1025-1063.
3. BoMed Ltd. Prepare the patient. In: BoMed Ltd, eds. NCCOM3R7S Cardiodynamic Monitor Operator's Manual Irvine, CA: BoMed
Ltd, 1991; 15-17.
4. Imholz BP, van Montfrans GA, Settels J J, van der Hoeven GM,
Karemaker JM, Wieling W. Continuous non-invasive blood pressure
monitoring: reliability of Finapres device during the Valsalva
manoeuvre. Cardiovasc Res 1988; 22: 390-397.
5. Bernstein DP. A new stroke volume equation for thoracic electrical
bioimpedance: theory and rationale. Crit Care Med 1986; 14:
904-909.

6. Bland JM, Altman DG. Statistical methods for assessing agreement
between two methods of clinical measurement. Lancet 1986; i:
307-310.
7. Shannon RP, Maher KA, Santinga JT, Royal HD, Wei JY.
Comparison of differences in the hemodynamic response to passive postural stress in healthy subjects greater than 70 years and
less than 30 years of age. Am J Cardiol 1991 ; 67: t 110-1116.
8. Vaz M, Kurnar MV, Redrigues D, Kulkarni RN, Shetty PS.
Variability in cardiovascular and plasma norepinephdne responses
to head-up tilt in healthy human subjects. J Auton New Syst 1991;
36: 201-208.
9. Hainsworth R, AI-Shamma YM. Cardiovascular responses to
upright tilting in healthy subjects. Clin Sci 1988; 74:17-22.
10. Matalon SV, Farhi LE. Cardiopulmenary readjustments in passive
tilt. Appl Physiol 1979; 47: 503-507.
11. Tuckman J, Shillingford J. Effect of different degrees of tilt on cardiac output, heart rate and blood pressure in normal man. Br Heart
J 1966; 28: 32-39.
12. de Mey C, Enterling D. Variant responses impair the usefulness of
passive upright tilt in drug research. Methods Find Exp Clin
Pharmaco11988; 10: 57-64.
13. de Mey C, Enterling D, Brendel E, Meineke I. Postprandial changes
in supine and erect heart rate, systemic blood pressure and plasma
noradrenaline and renin activity in normal subjects. Eur J Clin
Pharmaco11987; 32: 471-476.
14. Parati G, Casadei R, Groppelli A, Di Rienzo M, Mancia G.
Comparison of finger and intra-arterial blood pressure monitoring at
rest and during laboratory testing. Hypertension 1989; 13: 647-655.
15. Van Egmond J, Hasenbos M, Crul JF. Invasive v. non-invasive
measurement of arterial pressure. Comparison of two automatic
methods and simultaneously measured direct intra-arterial pressure. Br J Anaesth 1985; 57: 434-444.
16. Critchley LA, Short TG, Gin T. Hypotension during subarachnoid
anaesthesia: haemodynamic analysis of three treatments. Br J
Anaesth 1994; 72: I51-155.
17. Sanders DJ, Jewkes CF, Sear JW, Verhoeff F, Foex P. Thoracic
electrical bioimpedance measurement of cardiac output and cardiovascular responses to the induction of anaesthesia and to laryngoscopy and intubation. Anaesth 1992; 47: 736-740.
18. Thomas SH. Impedance cardiography using the Sramek-Bernstein
method: accuracy and variability at rest and during exercise. Br J
Clin Pharmacol 1992; 34: 467-476.
19. Vohra A, Thomas AN, Harper NJ, Pollard BJ. Non-invasive measurement of cardiac output during induction of anaesthesia and tracheal intubation: thiopentone and propofol compared. Br J Anaesth
1991 ; 67: 64-68.
20. Bernstein DP. Noninvasive cardiac output measurement. In:
Shoemaker WC, ed. Textbook of Critical Care. London: Saunders,
1989; 159-185.
21. Gotshall RW, Wood VC, Miles DS. Comparison of two impedance
cardiographic techniques for measuring cardiac output. Ann
Biomed Engineer 1989; 17: 495-505.
22. Wong DH, Tremper KK, Stemmer EA et aL Noninvasive cardiac
output: simultaneous comparison of two different methods with
thermodilution. Anesthesiology 1990; 72: 784-792.
23. Young JD, McQuillan P. Comparison of thoracic electrical bioimpedance and thermodilution for the measurement of cardiac index
in patients with severe sepsis. Br J Anaesth 1993; 70: 58-62.
24. Coonan T J, Hope CE. Cardio-respiratory effects of change of body
position. Can Anaesth Soc J 1983; 30: 424-438.

Clinical Autonomic Research * vol 7 ~ 1997

101