Assessment of Pulse Transit Time To Indicate Cardiovascular Changes During Obstetric Spinal Anaesthesia

Download as pdf or txt
Download as pdf or txt
You are on page 1of 6

British Journal of Anaesthesia 96 (1): 1005 (2006)

doi:10.1093/bja/aei266

Advance Access publication October 28, 2005

Assessment of pulse transit time to indicate cardiovascular


changes during obstetric spinal anaesthesiay
G. Sharwood-Smith*, J. Bruce and G. Drummond
Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary of Edinburgh,
Edinburgh EH16 4SU, UK
*Corresponding author. E-mail: gssmith@staffmail.ed.ac.uk
Background. Pulse transit time (PTT) measurement may provide rapidly available beat-to-beat
cardiovascular information when conditions change quickly and routine invasive arterial pressure
measurement is not justified, for example during obstetric spinal anaesthesia.

Results. We analysed data from 58 normotensive patients and 15 patients with pregnancyinduced hypertension (PIH). PTT increased with the onset of spinal anaesthesia as arterial pressure decreased. An increase of 20% in PTT was 74% sensitive and 70% specific in indicating
a decrease in mean arterial pressure of more than 10%. Changes in PTT were related to changes
in mean arterial pressure (r2=0.55, P<0.0001). Arterial pressure changes were greater and PTT
increased significantly more quickly in the normotensive patients than in the patients with
hypertension [median, quartiles: 32 (14, 56) ms min1 compared with 7 (6, 18) ms min1;
P<0.01, MannWhitney U-test]. However, the relationship between PTT and arterial pressure
was similar for the normotensive patients and the patients with PIH.
Conclusion. PTT measurement gave a beat-to-beat indication of arterial pressure during spinal
anaesthesia, and could be developed to allow prediction of the onset of hypotension.
Br J Anaesth 2006; 96: 1005
Keywords: anaesthesia, obstetric; anaesthetic techniques, regional, spinal; cardiovascular
system; monitoring, pulse transit time; pregnancy
Accepted for publication: September 24, 2005

In clinical conditions, arterial pressure may change so


quickly that intermittent non-invasive measurements may
be too slow and inaccurate to allow early detection and
prompt treatment, especially in obese subjects. However,
routine invasive measurement may be inappropriate, for
example in obstetric spinal anaesthesia, where hypotension
is the most frequent complication and poses risks to both
mother and foetus. In conscious subjects, arm movement can
delay the display of an arterial pressure reading through two
or three measurement cycles, often at a time when changes
may be considerable. An additional non-invasive measurement that could give early warning of arterial pressure
change would be useful clinically.
Pulse transit time (PTT) measurement offers beat-to-beat
cardiovascular information.1 Such measurements have been
used previously to infer changes in autonomic activity2 and
arterial pressure.3 PTT, measured as the interval from the

ECG R wave to the pulse plethysmograph upstroke, was


used recently to assess cardiovascular responses to anaesthesia and intubation.4 Both the ECG and the plethysmograph wave can be obtained from standard monitoring
equipment. We used a custom-built analogue device to
acquire automatically the interval between the ECG R
wave and the pulse plethysmograph upstroke.
PTT is of clinical interest as an index of arterial stiffness
and hence of arterial pressure,3 5 since arterial stiffness
increases as arterial pressure increases.68 However, other
factors may affect arterial stiffness. For example, recent
studies suggest that hypotension following spinal
y

Data from this study were presented in part at the Obstetric Anaesthetists Association Meeting at Nottingham, UK, on May 10, 2002 and
at the 13th World Congress of the International Society for the Study of
Hypertension in Pregnancy at Toronto, Canada, on June 2, 2002.

 The Board of Management and Trustees of the British Journal of Anaesthesia 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Downloaded from http://bja.oxfordjournals.org/ by guest on March 18, 2016

Method. We obtained ethics approval for an observational study of PTT during the onset of
spinal anaesthesia in patients having elective or urgent Caesarean section. PTT was measured
as the difference in time between the peak of the ECG R wave and the upstroke of the toe
plethysmograph. Arterial pressure was measured by non-invasive sphygmomanometry.

Pulse transit time during obstetric spinal anaesthesia

anaesthesia is less likely in patients with pregnancy-induced


hypertension (PIH) than in normotensive patients.9 Changes
in PTT following spinal anaesthesia may indicate differences in arterial stiffness in these patients.
The prime aim of this study was to observe PTT in a
clinical scenario where sudden onset of hypotension is
relatively frequent, and assess its value for predicting
such changes. A secondary aim was to compare the
responses of patients with and without PIH.

Methods

Results
Ninety-two patients were studied; we obtained data suitable
for analysis from 58 normotensive patients and 15 with PIH.
There were no obvious systematic differences in the reasons
for exclusion between the two groups of patients (Table 1).
The two groups were similar in respect of height and weight,
but, as might be expected, heart rate was less, arterial pressure was greater and gestational age was less in the patients
with PIH (Table 2). Before the spinal anaesthetic, normotensive patients were given 400 (300, 500) ml of
Hartmanns solution and the patients with PIH received
150 (100, 225) ml. The dose of bupivacaine was 13
(12.5, 13.5) mg in both the normotensive and the hypertensive patients. Most patients received diamorphine 300 mg, but
nine were given 400 mg. Ephedrine had to be given to 46 of
the normotensive patients and three of the patients with PIH
(P<0.001); other vasopressor and vagolytic agents
(phenylephrine, atropine and glycopyrollate) were also
used more frequently in the normotensive patients.
Data from five patients were not analysed because
vasopressor drugs were given prophylactically by personal
preference of the anaesthetist immediately after spinal

Table 1 Reasons for exclusion from analysis

Total number before exclusions


Reasons for exclusion
Inadequate data
Vasopressor given prophylactically
Computer failure
Conversion to general anaesthetic
Insulin-dependent diabetes
Essential hypertension
Number of patients analysed

101

Normotensive

PIH

74

18

9
5
1
1
0
0
58

1
0
0
0
1
1
15

Downloaded from http://bja.oxfordjournals.org/ by guest on March 18, 2016

The local ethics committee approved collection and recording of data from routine cardiovascular monitoring devices,
but not the modification of routine management in any other
way. We obtained informed verbal consent for the data
collection. We recorded PTT during the onset of spinal
anaesthesia in non-labouring women having Caesarean section for routine elective or urgent indications. Patients were
recruited as they presented over a 6-month period; of these,
74 were normotensive. Eighteen patients had severe PIH,
defined using standard criteria10 as hypertension which
developed after 20 weeks of gestation and required antihypertensive medication with nifedipine, labetalol or
methyldopa, singly or in combination. We included patients
with or without proteinuria. We undertook this study before
our unit introduced i.v. magnesium sulphate treatment for
severe PIH.
The values were obtained from before the spinal anaesthetic to the time the patient was ready for surgery. Vasopressor or vagolytic drugs were given by the clinician
managing the anaesthesia, according to normal practice,
in response to changes in arterial pressure, heart rate, or
the onset of symptoms suggestive of hypotension, such as
dizziness, nausea or vomiting. Some of these clinicians did
not routinely give vasopressor agents prophylactically,
others did, and some gave them occasionally.
Patients were placed in a supine wedged position and an
infusion of Hartmanns solution was started. ECG monitoring and an automated arterial pressure (NIBP) recording cuff
were applied (Cardiocap 2; Datex). The baseline arterial
pressure was recorded as the mean of three measurements
taken at 2-min intervals. An oximeter probe was placed on
the second toe of the left foot. Spinal anaesthesia was then
administered with the patient in either the sitting or left
lateral position. A 24 gauge Sprotte needle was used to
give between 2.5 and 2.7 ml of hyperbaric bupivacaine
0.5% with diamorphine 0.3 or 0.4 mg according to the
anaesthetists preference. The patient was then returned to
the wedged supine position. The time was recorded, and the
events that were marked electronically included the following: the connection of monitoring equipment; the initial
change of position for the spinal; the return to a wedged
supine position; the administration of vasopressor or other
i.v. drugs; and the transfer of the patient to the operating
theatre. IV fluids given before spinal anaesthesia and the

total given over the study period were recorded. Heart rate
and NIBP were recorded at 2-min intervals. The ECG and
photoplethysmograph signals from the analogue output of
the Cardiocap monitor were transferred to a purpose-built
analogue computer constructed by Leiden University. This
computed the time between the peak of the ECG R wave and
the maximum rate of the plethysmograph wave upswing.
The time intervals and digital signals from the Datex monitor were recorded in digital form on a Satellite Pro 4300
(Toshiba) laptop computer.
Before data analysis, spurious ECG and photoplethysmograph signals generated by patient movement were removed.
These artefacts were defined using an Excel function (Excel
version 9.0, 1999; Microsoft, Redmond, WA, USA) as values that were 20% less or greater than the rolling mean
PTT, and were filtered from the data before analysis.
Statistical analysis was with GraphPad Prism version 3.02
and Analyse-It software for Excel, version 1.71 (Analyse-it
Software, Leeds, UK). Data are presented as medians
(quartile values) unless stated otherwise.

Sharwood-Smith et al.

Table 2 Patient details and cardiovascular measurements before and after spinal anaesthesia. Values are median (interquartile values). ns, not significant. Students
t-test, *P<0.05, **P<0.0001; MannWhitney U-test, #P<0.01
Pregnancy-induced hypertension

58
32 (30, 35)
162 (158, 168)
70 (61, 78)
39 (39, 39)

15
32 (30, 37)
162 (160, 170)
72 (62, 83)
36 (33, 38)

89 (78, 102)

80 (74, 94)

99 (91, 104)
126 (118, 138)
390 (345, 422)

115 (104, 119)


144 (138, 160)
353 (325, 399)

**
**
*

87 (78, 109)

80 (71, 101)

ns

92 (86, 99)
124 (116, 136)
413 (373, 454)

106 (98, 111)


140 (136, 154)
370 (342, 417)

**
ns
*

Measurements at greatest pulse transit time or first intervention


Heart rate (beats min1)
96 (78, 109)
Mean arterial pressure (mm Hg)
77 (66, 90)
Change in mean arterial pressure
18 (5, 33)
Systolic arterial pressure (mm Hg)
106 (92, 120)
Pulse transit time (ms)
488 (429, 532)
Greatest change in PTT (ms)
94 (62, 123)
Greatest change in PTT (%)
24%
Rate of change in PTT (ms min1)
32 (14, 56)
Time to greatest PTT change (min)
2.4 (1.4, 3.4)

79 (75, 98)
89 (98, 111)
22 (11, 29)
119 (111, 134)
417 (389, 495)
75 (54, 118)
21%
7 (6, 18)
5.0 (3.2, 7.7)

ns
**
ns
ns
*
ns
ns
#
#

Minimum arterial pressure after spinal anaesthesia


Mean
Systolic

83 (78, 95)
116 (108, 126)

**
**

Cardiovascular values
Before spinal anaesthesia
Heart rate (beats min1)
Arterial pressure (mm Hg)
Mean
Systolic
Pulse transit time (ms)
After spinal anaesthesia
Heart rate (beats min1)
Arterial pressure (mm Hg)
Mean
Systolic
Pulse transit time (ms)

69 (60, 78)
97 (87, 108)

Doses of ephedrine 6 mg
Doses of atropine
Doses of phenylephrine
700

Spinal

600

Sitting

500
400
150
300
100

200

50

100
0

Arterial pressure (mm Hg)

anaesthesia and before PTT and arterial pressure recordings


could be obtained. A standardized format of clinical practice
was not imposed in this observational study. In 10 patients,
technical problems with recording either PTT or arterial
pressure yielded insufficient data for analysis.
Mean arterial pressure (MAP) before spinal anaesthesia
was 99 (91, 104) mm Hg in the normotensive patients and
115 (104, 119) mm Hg in patients with PIH. With the onset
of spinal anaesthesia, MAP decreased by 18 (5, 33) and
22 (11, 29) mm Hg in normotensive and PIH patients
respectively.
Patient movement and repositioning after carrying out the
block disturbed the ECG and plethysmograph signals, and
could cause spurious PTT values. These were less than 3%
of the total values obtained. Before anaesthesia, PTT was
significantly less in the patients with PIH: 353 (325, 383) ms
(P<0.05) compared with 390 (346, 417) ms in the normotensive group (P<0.05). PTT changed during the onset
of spinal anaesthesia (Fig. 1) by 24% in the normotensive
group and 21% in the PIH group. The greatest change in PTT
occurred 2.4 (1.4, 3.4) min after spinal anaesthetic in the
normotensive group and 5.0 (3.2, 7.7) min after spinal anaesthetic in the hypertensive group. Thus, PTT increased more
rapidly in the normotensive patients [32 (14, 56) ms min1]

PTT (ms) and heart rate


(beats min1)

Patient details
Number
Age
Height (cm)
Weight (kg)
Gestation (weeks)

Significance

0
10

15

20
Time (min)

25

30

Fig 1 An example of patient responses. Upper, continuous trace: pulse


transit time (ms). Lower, discontinuous trace: heart rate calculated from
successive R-R intervals. Systolic and diastolic arterial pressures are shown
as vertical bars and arrowheads.

than in the patients with PIH [7 (6, 18) ms min1] (P< 0.01,
MannWhitney U-test).
The relationship between PTT and MAP was examined
before and after spinal anaesthesia (Fig. 2). There was a

102

Downloaded from http://bja.oxfordjournals.org/ by guest on March 18, 2016

Normotensive subjects

Pulse transit time during obstetric spinal anaesthesia

A 800

Normotensive patients
PIH patients

Pulse transit time (ms)

PTT (ms)

550

600

400

200

450

350

250
50

100
Mean arterial pressure (mm Hg)

150

50

60

70
80
90 100 110 120
Mean arterial pressure (mm Hg)

130

140

Fig 3 Comparison of the linear regression relationships of pulse transit time


and mean arterial pressure in normotensive subjects and patients with
pregnancy-induced hypertension. The outer lines represent the 95% confidence interval for the regression.

B 800

PTT (ms)

100
400

Sensitivity (%)

80

200
50

100
Mean arterial pressure (mm Hg)

150

Fig 2 Relationship of pulse transit time to mean arterial pressure in (A)


normotensive subjects and (B) patients with pregnancy-induced hypertension. The open symbols are before and the closed symbols after spinal
anaesthesia. The linear regression relationships are shown with the 95%
confidence interval for the line. Both relationships are significant
(P<0.0001).

significant correlation in both the normotensive (r2=0.55,


P<0.0001) and the PIH group (r2=0.45, P<0.0001)
(Fig. 3). The slopes of the relationships between PTT and
MAP were not different when normotensive and hypertensive subjects were compared [slopes (95% confidence interval, CI) were 3.12 (3.64, 2.59) and 2.88 (4.12,
1.64) ms (mm Hg)1 respectively].
We examined the sensitivity and specificity of changes in
PTT to indicate the onset of hypotension. The resulting
receiver operating characteristic (ROC) curves for decreases
in MAP of 5 and 10% are given in Figure 4. For a decrease in
MAP of 5%, an increase of 10% in PTT was 95% sensitive
but only 15% specific. If a cut-off value of a 20% increase in
PTT was taken, the sensitivity and specificity were 69 and
77% respectively. The area under the ROC curve was 0.79
(95% CI, 0.680.9; P<0.001 compared with an area of 0.5).
Considering decreases in MAP of more than 10%, an
increase of 20% in PTT was 74% sensitive and 70% specific.
The area under the ROC curve was 0.72 (95% CI, 0.600.85;
P<0.001 compared with an area of 0.5).

60

40

20
5% decrease in mean arterial pressure
10% decrease in mean arterial pressure

0
0

20

40
60
1-Specificity (%)

80

100

Fig 4 Receiver operating characteristic curves for changes in pulse transit


time in relation to a decrease in mean arterial pressure by 5 and 10%. For the
5% decrease, the area under the curve is 0.79 (0.680.90) and for the 10%
decrease the area is 0.73 (0.600.85) (95% confidence intervals) Both areas
are significantly greater than 0.5 (P<0.001).

Discussion
To our knowledge, the relationship between PTT and arterial
pressure has not previously been studied systematically
during obstetric spinal anaesthesia. We chose to study
this scenario because rapid and substantial changes in arterial pressure are relatively frequent. We found that changes in
PTT were related to arterial pressure changes and that the
relationship between PTT and arterial pressure was the same
in normotensive patients and those with PIH.
We measured the time interval between the ECG R wave
and the upsweep of the plethysmograph.11 12 This time
includes two principal components, the time between electrical activation of the ventricle and cardiac ejection, and the

103

Downloaded from http://bja.oxfordjournals.org/ by guest on March 18, 2016

600

Sharwood-Smith et al.

time taken for the resultant pressure wave to be transmitted


along the artery to generate the plethysmograph upstroke.11
The time from ventricular activation to cardiac ejection
depends upon a number of factors related to preload,
heart rate and contractility.13 14 This time is small compared
with the time taken for pulse wave transmission along the
vessel, particularly in young normotensive patients.
Consequently, the greater part of the PTT we measured
indicates vascular elastance according to the Bramwell
Hill relationship15 described for the velocity of pressure
waves:
p
Velocity DP=V=DVr

104

Downloaded from http://bja.oxfordjournals.org/ by guest on March 18, 2016

where r is the density of blood and DP/[V/DV] is the


specific elastance of the vessel. The pressurevolume
relationship of arteries is non-linear: as pressure decreases,
elastance decreases, pulse wave velocity decreases and PTT
is increased, as we have confirmed. Other factors that affect
vascular elastance, such as hypertension and change in
sympathetic activation, could also affect PTT, but these
influences are disputed. For example, although ultrasound
estimates of radial artery elastance suggest that arterial
infusion of phenylephrine can increase elastance,16 others
have concluded that greater arterial elastance in hypertensive patients can be explained entirely by differences in
arterial pressure.7 17 These findings are supported by the
present study, in which we found no discernible difference
between normotensive patients and those with PIH in the
relationship for arterial pressure and PTT. We conclude
that the mechanical properties of the large conducting
vessels in patients with this condition are not affected,
whereas the resistance vessels are clearly affected. This
finding is not altogether unexpected: the site of modulation of arterial resistance depends upon the type of
stimulus.18
The shape of the pressure waveform in peripheral arteries
varies considerably with age and disease.19 The rate of
increase of the pressure varies considerably with age, but
in the limited range of ages that we studied this could not
cause much variation.
The analogue device that we used detected the maximum
rate of change of the plethysmograph waveform. In preliminary unpublished studies of healthy volunteers, we used a
method of intersecting tangents to determine the nadir of the
plethysmograph waveform. Measurements of PTT using this
nadir were less affected by changes in heart rate than measurements made using the time to the maximum rate of
change of the plethysmograph signal. These findings confirm those of others.20 However, this method was not compatible with analogue preprocessing, in that we not could
detect the maximum rate of change of the plethysmograph
wave. It was therefore not practical for this study. Thus, one
source of variation in the relationship between PTT and
arterial pressure could result from heart rate changes and
the method used by our analogue detector.

There is a difference in time between the occurrence of


plethysmograph waveforms in the finger and toe because of
differences in distance along the arteries. Epidural anaesthesia increases this time difference and was attributed by
the investigators to sympathetic blockade in the leg arteries.21 However, the time difference only increased between
10 and 20% and this increase was accompanied by a
decrease in arterial pressure. Consequently, an equally
plausible alternative explanation is that hypotension, causing a proportional increase in pulse wave transmission time,
would have a greater absolute effect in the longer vessel.
This effect can account for the changes reported by these
workers.
Recently, marked changes in PTT were described during
general anaesthesia in association with tracheal intubation,
and these changes were attributed to autonomic activation.4
However, no measurements of arterial pressure were reported. Once again, the changes could have been caused by
changes in arterial pressure, because the hypertensive
response to insertion of the tracheal tube will increase arterial elastance and reduce PTT, as the authors reported.
Monitoring by means of PTT has been compared with
invasive arterial pressure measurements. If the directly
measured pressure changed by more than 10 mm Hg,
then PTT accurately tracked the change on 67% of occasions. However, the authors of this study concluded that PTT
did not have sufficient accuracy to replace direct arterial
measurements.22
Clinically, PTT changes are of interest as a non-invasive
beat-to-beat index of arterial pressure changes. Increased
arterial pressure itself causes increased arterial stiffness
but the relationship is non-linear at high and low pressures.23
In the present study, by using a large control group, in which
there were considerable changes in PTT, we found a correlation between MAP and PTT changes. More than 50% of
the variance in PTT is explained by the value of the MAP.
The remainder of the variance must result from other factors,
such as patient size, variation in accuracy of estimates of
both arterial pressure and PTT, and individual variations in
vessel wall characteristics. Arterial behaviour can be altered
by obesity,24 longitudinal tension25 and vasoactive mediators.16 Although these additional factors increase the variation between subjects, it is likely that they will not influence
the variation within an individual, so PTT can be a useful
measure of moment-to-moment changes within a particular
patient.
Our results were obtained in pregnant subjects, and the
mechanical properties of large vessels such as the aorta can
be affected by hormonal changes such as may occur in
pregnancy.26 However, the vascular changes of PIH are
probably confined to small resistance vessels,27 28 explaining
the similar relationship between PTT and arterial pressure in
normotensive and PIH patients.
Non-invasive methods for arterial pressure measurement,
such as automated sphygmomanometers, frequently fail to
display values when patient movement causes interference.

Pulse transit time during obstetric spinal anaesthesia

This is a particular problem in obstetric anaesthesia, where


the subjects are awake and may be agitated and the procedures are often urgent, with little opportunity for careful cuff
application and even less for arterial cannulation. We found
that PTT could potentially be used, in these circumstances,
to predict the onset of hypotension. The sensitivity and specificity are sufficient to indicate instantaneously changes in
arterial pressure and provide a rapid, non-invasive, withinsubject indication of hypotension. This may be of considerable value if invasive monitoring is not justified. We found
no evidence that the properties of large arteries are affected
by PIH.

Acknowledgements
We thank Professor A. Dahan, University of Leiden, for the loan of the
analogue computer for processing the ECG and optical plethysmograph
signals (Ajax). This study was supported by a grant from the Obstetric
Anaesthetists Association.

12

13
14

15
16

17
18

1 Smith RP, Argod J, Pepin J-L, Levy PA. Pulse transit time: an
appraisal of potential clinical applications. Thorax 1999; 54:
4528
2 Weiss T, Del Bo A, Reichek N, Engelman K. Pulse transit time
in the analysis of autonomic nervous system effects on the
cardiovascular-system. Psychophysiology 1980; 17: 2027
3 Sawada Y, Yamakoshi K. A correlation analysis between pulse
transit time and instantaneous blood pressure measured indirectly by the vascular unloading method. Biol Psychol 1985; 21: 19
4 Singham S, Voss L, Barnard J, Sleigh J. Nociceptive and anaestheticinduced changes in pulse transit time during general anaesthesia.
Br J Anaesth 2003; 91: 6626
5 Landowne M. A method using induced waves to study pressure
propagation in human arteries. Circ Res 1957; 5: 594601
6 Bramwell JD, Downing AC, Hill AV. The effect of blood pressure
on the extensibility of the human artery. Heart 1923; 10: 28995
7 Gribbin B, Pickering TG, Sleight P. Arterial distensibility in normal
and hypertensive man. Clin Sci 1979; 56: 4137
8 Schulze-Bauer CAJ, Holzapfel GA. Determination of constitutive
equations for human arteries from clinical data. J Biomech 2003;
36: 1659
9 Clark VA, Sharwood-Smith GH, Stewart AVG. Ephedrine
requirements are reduced during spinal anaesthesia for caesarean
section in preeclampsia. Int J Obstet Anaesth 2005; 14: 913
10 Davey DA, MacGillivray I. The classification and definition of the
hypertensive disorders of pregnancy. Am J Obstet Gynecol 1988;
158: 8928
11 Steptoe A, Godaert G, Ross A, Schreurs P. The cardiac and
vascular components of pulse transmission time: a computer

105

20

21

22

23

24

25

26

27

28

Downloaded from http://bja.oxfordjournals.org/ by guest on March 18, 2016

19

References

analysis of systolic time intervals. Psychophysiology 1983; 20:


2519
Bugram R, Akhlaghi-Farsi H, Maresch H, Pfurtscheller G. A
method for determining pulse transmission time. Biomed Tech
1994; 39: 516
Weissler AM, White GD, Harris LC. Left ventricular ejection time
index in man. J Appl Physiol 1963; 18: 91931
Weissler AM, Peeler RG, Roehll WH Jr. Relationships between
left ventricular ejection time, stroke volume, and heart rate in
normal individuals and patients with cardiovascular disease.
Am Heart J 1961; 62: 36774
Bramwell JC, Hill AV. The velocity of the pulse wave in man. Proc R
Soc B 1922; 93: 298306
Grassi G, Giannattasio C, Failla M, et al. Sympathetic modulation
of radial artery compliance in congestive heart failure. Hypertension 1995; 26: 34854
Laurent S. Arterial wall hypertrophy and stiffness in essential
hypertensive patients. Hypertension 1995; 26: 35562
Folkow B, Sonnenschein RR, Wright DL. Loci of neurogenic and
metabolic effects on precapillary vessels of skeletal muscle.
Acta Physiol Scand 1971; 81: 45971
McLean CE, Clason WPC, Stoughton PV. The peripheral pulse as
a diagnostic tool. Angiology 1964; 14: 22131
Chiu YC, Arand PW, Shroff SG, Feldman T, Carroll JD. Determination of pulse-wave velocities with computerized algorithms.
Am Heart J 1991; 121: 146070
Babchenko A, Davidson E, Adler D, Ginosar Y, Kurz V, Nitzan M.
Increase in pulse transit time to the foot after epidural anaesthesia
treatment. Med Biol Eng Comput 2000; 38: 6749
Young CC, Mark JB, White W, DeBree A, Vender JS, Fleming A.
Clinical evaluation of continuous noninvasive blood pressure
monitoring: accuracy and tracking capabilities. J Clin Monit
1995; 11: 24552
Schulze-Bauer CAJ, Holzapfel GA. Determination of constitutive
equations for human arteries from clinical data. J Biomech 2003;
36: 1659
Toto-Moukouo JJ, Achimastos A, Asmar RG, Hugues CJ, Safar ME.
Pulse wave velocity in patients with obesity and hypertension.
Am Heart J 1986; 112: 13640
Wang YY, Jan MY, Wang GC, Bau JG, Wang WK. Pressure pulse
velocity is related to the longitudinal elastic properties of the
artery. Physiol Meas 2004; 25: 1397403
Chelsky R, Wilson RA, Morton MJ, et al. Alteration of ascending
thoracic aorta compliance after treatment with menotropin.
Am J Obstet Gynecol 1997; 176: 12559
McCarthy AL, Woolfson RG, Raju SK, Poston L. Abnormal
endothelial cell function of resistance arteries from women
with preeclampsia. Am J Obstet Gynecol 1993; 168: 132330
Suzuki Y, Kajikuri J, Suzumori K, Itoh T. Mechanisms underlying
the reduced endothelium dependent relaxation in human omental
resistance artery in pre-eclampsia. J Physiol (Lond) 2000; 527:
16374

You might also like