Stroke. 1997;28:1195-1197
(Stroke. 1997;28:1195-1197.)
© 1997 American Heart Association, Inc.
Effect of Pco2 Changes Induced by Head-Upright Tilt on Transcranial Doppler Recordings
Simone Cencetti, MD;
Gabriele Bandinelli, MD;
Alfonso Lagi, MD
From the Department of Internal Medicine 1, S Maria Nuova Hospital,
Florence, Italy.
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Abstract
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Background and Purpose Transcranial
Doppler (TCD) monitoring
of mean blood flow velocity (mV) during
head-upright tilt can
allow testing of cerebral autoregulation.
Nonetheless, head-upright
tilt can induce changes in the
ventilation-perfusion relationship
and/or respiratory activity that
might influence TCD data.
Methods Forty-eight healthy volunteers underwent
monitoring of mV and end-tidal CO2 in the horizontal
position and during head-upright tilt.
Results Both mV and end-tidal CO2
significantly decreased in orthostasis (P<.01). Linear
regression analysis showed a significant linkage between
end-tidal CO2 and mV changes (r=.83,
P<.01).
Conclusions Changes in ventilation-perfusion ratio
and in the respiratory pattern induced by head-upright tilt can
significantly influence TCD data by determining a
PCO2 decrease.
Key Words: blood flow velocity carbon dioxide cerebral blood flow hemodynamics ultrasonics
 |
Introduction
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Transcranial
Doppler (TCD) has been widely used to investigate
cerebral
hemodynamics and cerebral autoregulation in response
to
changes in systemic hemodynamics induced by several
different
methods, including postural stimuli.
1 2 3 4
Orthostasis can
induce changes in the respiratory pattern and
especially the
ventilation-perfusion ratio, thus determining changes in
P
CO2.
Because the effect of
P
CO2 change on TCD recordings of mean
blood
flow velocity (mV) has been well documented,
5 the
present study
aimed to test whether slight changes of the
respiratory-perfusion
pattern induced by head-upright tilt (HUT) can
affect the interpretation
of TCD data in orthostasis.
 |
Subjects and Methods
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Forty-eight healthy men (mean age, 38.8 years; range, 22 to
50
years) gave their informed consent to the study, which was
approved by
the local ethics committee. All the subjects were
free from
hypertension, diabetes, cerebrovascular disease, and
significant
stenosis of intracranial and extracranial cerebral
arteries, as
shown by physical examination, clinical history,
and preliminary
ultrasonographic investigations. All the subjects
were tested in the
afternoon; each subject was lying on a proper
tilt table, and the room
temperature was kept constant at 20°C
to 22°C. After the subjects
had rested for 20 minutes, the
devices for noninvasive monitoring of
the chosen biological
parameters were positioned.
Recordings of cerebral blood flow
velocity were performed with
a 2-MHz probe (Multidop L, DWL)
on the middle cerebral artery of the
dominant hemisphere; the
position of the probe was kept constant by
means of a mechanical
probe holder equipped with an elastic band that
was fastened
around the skull. The insonation depth was set between 51
and
57 mm, depending on the optimization and stability of the
signal,
and the horizontal sweep speed was 10 seconds. Continuous
end-tidal
CO
2 was measured with a capnographic monitor
(Capnogard, Novametrix)
while the subjects were spontaneously breathing
room air. Blood
pressure and heart rate were noninvasively monitored
(Finapres
Ohmeda). Respiratory activity was monitored by means of a
piezoelectric
transducer (OS-9000SRS, Goldstar) fastened around the
bottom
of the chest with an elastic band, as previously
described.
6 During TCD at the horizontal position, data
were collected
over approximately 20 consecutive cardiac cycles, at
least 5
minutes after the devices for noninvasive monitoring had been
applied,
when the monitored parameters reached a steady
state. The table
was then turned up at 60°, and recordings
were again performed
after at least 5 minutes. For each subject, mV and
end-tidal
CO
2 were calculated as mean values in each
position. Differences
between the horizontal and standing positions for
mV, end-tidal
CO
2, and rate of breathing were statistically
evaluated by paired
t test. Linear regression
analysis was performed between percent
changes of mV during HUT
and absolute changes (in millimeters
of mercury) of end-tidal
CO
2.
 |
Results
|
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Results of TCD and capnometry are shown as mean±SD in
the
Table

. During HUT, the subjects displayed a significant
drop
of end-tidal CO
2. mV values also showed a significant
drop during
HUT. Mean arterial blood pressure did not
change significantly
with HUT (92.6±13.0 mm Hg at baseline,
94.3±10.8
mm Hg during HUT); heart rate slightly increased (from
66.2±11.6
to 74.8±8.4 beats per minute;
P<.05). The rate
of
breathing did not change significantly in orthostasis (from
16.0±4.94
to 15.33±3.94 breaths per minute), although the
piezoelectric
transducer recorded wider expansions of the chest
wall in the
upright position (Fig 1

). Linear regression
analysis (Fig 2

)
showed a significant
(
r=.83;
P<.01) linkage between end-tidal
CO
2 and mV changes, expressed by a constant of 2.97
(percent mV
change/mm Hg).

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Figure 1. Continuous recordings of respiratory
activity and cardiovascular and cerebrovascular
parameters during head-upright tilt. Track 1, R-R interval
(in milliseconds) on electrocardiographic tracing; tracks 2 through 4,
diastolic, mean, and systolic arterial
pressures, respectively; tracks 5 through 7, diastolic,
mean, and systolic cerebral blood flow velocities,
respectively; track 8, respiratory activity; and track 9, marker. The
first two spikes on track 9 (interval, 20 seconds) indicate the
automatic movement of the tilt table from horizontal to a 60° upright
position.
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Figure 2. Scatterplot and regression line of the percent
changes of mean blood flow velocity (mV) for the corresponding absolute
PCO2 changes during head-upright
tilt.
|
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Discussion
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Head-upright tilt induced slight but significant drops in both
end-tidal
CO
2 and mV in the healthy subjects examined in
the present study.
The mV drop was mostly determined by end-tidal
CO
2 changes,
as demonstrated by the significant result of
linear regression
analysis, with a 2.97% change of mV for
each mm Hg change of
end-tidal CO
2, which is similar
to what was previously found
in other different studies.
7
Results for mV during HUT were
not affected by the autoregulatory
response because data were
collected at least 5 minutes after tilt,
when it is likely that
the dynamic autoregulatory response already was
completed.
8 Although the validity of TCD measurements
during HUT has been
questioned by some authors
2 because of
concerns about a possible
change in the diameter of the middle cerebral
artery during
HUT, further studies
3 demonstrated that such
changes of the
vessel cross-sectional diameter are negligible during
HUT. Because
the rate of breathing did not change significantly during
tilt,
the observed changes of end-tidal CO
2 values are
likely to depend
on changes of the ventilation-perfusion relationship
during
HUT. In fact, in the normal upright lung, the blood flow per
unit
volume decreases from bottom to top, reaching very low values
at
the apex, where perfusion is possible only during systole;
in addition,
ventilation, despite a less marked change, increases
from top to bottom
in the upright lung because of the wider
expansions of the bottom of
the chest wall that are allowed
by the upright position (Fig 1

). The
changes of the ventilation-perfusion
relationships during HUT result in
a sort of shunt effect that
does not affect blood oxygen saturation but
allows, at the bottom
of the lungs, a better clearance of
CO
2, which diffuses through
the membrane about 20 times as
rapidly as oxygen, thus inducing
a slight hypocapnia. The
results from the present study suggest
that TCD studies on cerebral
autoregulation in response to postural
stimuli should include careful
examination of end-tidal CO
2 values, at least if the data
analysis is performed as a comparison
between horizontal and
standing positions. Furthermore, the
results from the present study
stress the need for end-tidal
CO
2 monitoring to attempt to
explain the paradoxical constriction
described during presyncope in
some subjects,
9 since syncopal
subjects often show marked
changes in the respiratory pattern
during presyncope.
 |
Footnotes
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Reprint requests to Alfonso Lagi, MD, Via G Mameli 44, 50131
Firenze, Italy.
Received January 14, 1997;
revision received March 6, 1997;
accepted March 21, 1997.
 |
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