Vol. 274, Issue 5, H1590-H1597, May 1998
Step baroreflex response in awake patients undergoing carotid
surgery: time- and frequency-domain analysis
Giora
Landesberg1,
Dan
Adam3,
Yacov
Berlatzky2, and
Solange
Akselrod4
1 Departments of Anesthesiology
and Critical Care Medicine and
2 Vascular Surgery and
Transplantation, Hebrew University-Hadassah Hospital, Jerusalem 91120;
3 Department of Biomedical
Engineering, The Technion-Institute of Technology, Haifa 32000;
and 4 Department of Medical
Physics, Tel-Aviv University, Tel-Aviv 69978, Israel
 |
ABSTRACT |
Step baroreceptor stimulation can provide an
insight into the baroreflex control mechanism, yet this has never been
done in humans. During carotid surgery under regional anesthesia, a
step increase in baroreceptor stimulation occurs at carotid declamping immediately after removal of the intra-arterial atheromatous plaque. In
10 patients, the R-R interval and systolic and diastolic blood pressures (BP) were continuously recorded, and signals obtained within
the time window from 10 min before until 10 min after carotid declamping were analyzed. Mean ± SD time signals, power spectra, and transfer and coherence functions before and after declamping were
calculated. Immediately after carotid declamping, both heart rate (HR)
and BP declined in an exponential-like manner lasting 10.3 ± 5.9 min, and their power spectra increased in the entire frequency range.
Transfer function magnitude and coherence functions between BP and HR
increased predominantly in the midfrequency region (~0.1 Hz), with no
change in phase function. Thus, in carotid endarterectomy patients,
step increase in baroreceptor gain elicits a prolonged decline in HR
and BP. Frequency analyses support the notion that the baroreflex
control mechanism generates the midfrequency HR and BP variability,
although other frequency regions are also affected.
carotid baroreceptors; baroreflex control mechanism
| |
INTRODUCTION |
SYSTEM ANALYSIS of the human baroreflex control
mechanism (BCM) is extremely difficult for several reasons. The BCM is
a closed loop in the autonomic nervous system. It is strongly affected by various inputs from the central nervous system and is relatively inaccessible to direct and selective stimulation to its various elements, such as the baroreceptors. The heart rate (HR) and blood pressure (BP), often viewed as output signals of the baroreflex loop,
are also state variables and inputs in this loop, making analysis of
the system based on these parameters alone even more complex.
In humans, baroreflex "sensitivity" or gain is often estimated as
the maximal HR response to an incremental change in systolic BP induced
by intravenous injection of vasoactive drugs (e.g., phenylephrine and
nitroglycerin) (25). An alternative method utilizes the ratio of HR to
BP power spectra in the midfrequency (0.07-0.14 Hz), which is
considered to represent the activity of the BCM (3, 31). With these two
methods, it has been shown that patients with long-standing
cardiovascular diseases, i.e., hypertension, coronary artery disease,
congestive heart failure and diabetes mellitus, exhibit reduced
baroreflex sensitivity (15, 24, 28). Yet these measurements provide
only a narrow insight into the broad dynamic behavior of the BCM in
both health and disease.
Carotid endarterectomy surgery is frequently accompanied by hemodynamic
instability, believed to result from surgical stimulation of the
carotid baroreceptors (6, 27). We have previously shown (21) in
patients undergoing carotid endarterectomy under regional (cervical
block) anesthesia that HR and BP decline immediately after carotid
artery declamping and stabilize at a lower level. The most plausible
explanation for this phenomenon is a step increase in baroreceptor
stimulation secondary to the sudden distension and increased
pulsatility of the carotid artery after surgical removal of the stiff
intra-arterial plaque. In the present study, we further investigated
the HR and BP changes occurring during carotid artery declamping by
means of time- and frequency-domain analyses to shed more light on the
BCM in patients undergoing carotid endarterectomy.
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METHODS |
Patients, anesthesia, and surgery.
Ten of fifteen consecutive patients (7 men and 3 women) were included
in this study. Excluded only were patients with abnormal heart rhythm
(atrial fibrillation, multiple extrasystolic beats, or artificial
pacemaker; 2 patients) and those in whom a carotid shunt was used
intraoperatively because of the appearance of transient neurological
disturbance after carotid clamping (3 patients). The mean age was 67 ± 9 yr. Six patients suffered from chronic ischemic heart disease
(60%), seven had hypertension (70%), and three had diabetes mellitus
(30%). Most patients were on oral cardiovascular medications: nitrates
(2 of 10), calcium channel blockers (5 of 10), and 
-adrenergic
blockers (2 of 10). The study was approved by the institutional ethics
committee for human experimentation, and all patients gave their
informed consent.
Cervical block anesthesia was performed with a total of 25 ml of 0.5%
bupivacaine injected in the vicinity of cervical nerve roots
C2,
C3, and
C4. Surgery was carried out with
the patients fully awake and responsive. None of the patients suffered
from Horner's syndrome, hemodynamic or respiratory disturbances, or other complications as a result of the cervical block anesthesia. The
patients were monitored clinically throughout the procedure for any
sign or symptom of neurological deficit as well as by computerized
electroencephalogram (Cerebro-Trac 2500 SRD, Israel). None of the 10 patients exhibited any neurological disturbance during or after the
procedure.
The common carotid in the operated side, its bifurcation, and the
internal and external carotid arteries were dissected and separated
from the internal jugular vein and the vagus nerve, and after
administration of heparin (100 IU/kg iv), the common, internal, and
external carotid arteries were clamped. During carotid clamping, the
patient was carefully monitored for changes in neurological status,
with alteration in mental, verbal, or physical response necessitating
the immediate placement of a carotid shunt. The atheromatous plaque was
carefully excised from inside the artery via a longitudinal arteriotomy
incision across the bifurcation, leaving a clean and smooth surface in
the tunica media of the artery. The arteriotomy was then sutured, the
artery was flushed several times to ensure that no air or particulate
matter remained in its lumen, and the external and common carotid
artery clamps were removed first to avoid any possible embolization to
the brain. A few seconds later the internal carotid artery was also
declamped, and blood flow was restored to the brain. No vasoactive or
cardioactive drugs were used during the clamping and declamping of the
carotid artery unless the HR or systolic BP fell below 45 beats/min and 100 mmHg, respectively.
Data analysis.
The R-R interval (RRI) was obtained from lead II or lead V5 of the
electrocardiogram (ECG). The arterial BP waveform was obtained from an
intra-arterial (radial artery) catheter (20 gauge) and transmitted
through a fluid-filled tube connected to a transducer zeroed at the
level of the heart. Correct damping of this arterial-line system was
frequently checked using the fast-flush test (17) to avoid over- or
underdamping before recording the data. Both ECG and arterial BP
signals were recorded from the patient's monitor with a PC computer
using an analog-to-digital converter (AT-CODAS Dataq Instruments,
Keithley), a resolution of 12 bits, and a sampling rate of 250 samples/s for each signal. RRI and the systolic and diastolic data
points were detected with the aid of a "peak-and-trough" identification utility. The peak-and-trough points were then visually validated, and errors were manually corrected within the AT-CODAS software to improve data quality. The data were imported to MATLAB 4.2c
software (Math Works) for further signal processing.
The exact time of carotid artery declamping was recorded and used as
the common time (t = 0) for all
patients. A 20-min time window from 10 min before until 10 min after
declamping was linearly interpolated at a rate of 16 Hz for each signal
(RRI and systolic and diastolic BP). The means ± SD of RRI and
systolic and diastolic BP signals for all 10 patients in the 20-min
perideclamping time window were calculated. RRI and BP frequency-domain
analyses included power spectra and coherence and transfer functions
both before and immediately after carotid declamping. Frequency-domain
data from 8 of the 10 patients were averaged and included in the
statistical analysis. Two patients were excluded: one in whom the
afferent baroreceptor nerves were probably injured during surgery,
since no change in mean HR or BP trend or in their variability occurred after carotid declamping, and one in whom a very rapid decline (within
<4 min) in HR and BP occurred after carotid declamping, requiring
prompt pharmacological intervention, which interfered with the primary
HR and BP response.
We used Welch's averaged periodogram algorithm for computing the power
spectrum, cross-spectrum, and coherence and transfer functions (40).
Epochs of 512-s duration of interpolated RRI and systolic and diastolic
BP signals from both before and after carotid artery declamping were
divided into nine overlapping segments of 128 s each. The segments were
detrended (a linear trend was subtracted), Hanning windowed, and fast
Fourier transformed, using common MATLAB routines. The periodograms
were averaged to produce the spectrum estimate. The frequency
resolution obtained was 0.0078 Hz. For the purpose of statistical
comparison between the pre- and postdeclamping power spectra, each
patient's power spectral density (PSD) functions were normalized to
his or her own predeclamping total power. The frequency
( f ) range (0-0.45 Hz)
was divided into three regions, low
( f < 0.07 Hz), mid (0.07 
f 0.14 Hz), and high (0.14 < f 0.45 Hz), and the normalized
regional power (area under power spectrum curve in each frequency
region) was calculated. Paired t-test
analysis was used for statistical comparisons between the pre- and
postdeclamping power spectra for each of the frequency regions.
Coherence and transfer functions were similarly calculated by using
Welch's algorithm of averaging the results obtained from the nine
overlapping segments. Repeated-measures ANOVA (Duncan's multiple range
test) was used to compare between the post- and predeclamping transfer
and coherence functions (SPSS for Windows 5.01).
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RESULTS |
Time-domain results.
Carotid artery declamping was associated with an exponential-like
decline in both HR and BP in 9 of the 10 patients. In only one patient
were HR and BP not affected and remained unchanged after carotid
declamping. Figure 1 displays HR (RRI) and
systolic BP response to carotid artery declamping in a representative
patient. The mean ± SD RRI and systolic and diastolic BP trends for
all 10 patients from 10 min before up to 10 min after carotid
declamping are presented in Fig. 2. A slow
decline in both HR and BP is evident after declamping. The time elapsed
from carotid artery declamping to stabilization of HR and BP at lower
levels was 10.3 ± 5.9 min. If an exponential decline is assumed,
the mean ± SD time constant of HR and BP decline was 6.5 ± 3.7 min, the time constant defined as the time at which HR and BP achieved
1 
(1/e) of their measured plateau value.
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Fig. 1.
R-R interval (RRI) and systolic blood pressure (BP) trends during
carotid endarterectomy in a typical patient from study.
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Fig. 2.
Mean ± SD RRI and systolic and diastolic BP trends during carotid
artery declamping of 10 patients; t = 0 is exact time of carotid declamping in all patients.
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Frequency-domain results.
Figure 3 presents mean (and mean + SD)
normalized pre- and postdeclamping PSD of eight patients. Mean PSD was
higher after declamping compared with that before declamping over the
entire frequency range (0 < f < 0.5 Hz) in both RRI and BP signals. Table 1
shows that there was a statistically significant increase in total
power after declamping in all three frequency regions (low, mid, and
high) in both HR- and BP-related signals, except for the low and
midfrequencies in the diastolic BP.
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Fig. 3.
Pre- and postdeclamping normalized power spectra of RRI, systolic and
diastolic BP, and pulse pressure. In each panel, bottom 2 curves
represent mean (bottom solid curve) and mean + SD
(bottom dashed curve) normalized predeclamping spectra, and
top 2 curves correspond to postdeclamping mean (top solid
curve) and mean + SD (top dashed curve) spectra.
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The mean systolic and diastolic BP to RRI coherence and transfer
functions averaged for eight patients before and after carotid artery
declamping are presented in Fig 4. Figure
5 demonstrates the mean and 25th and 75th
percentiles of the difference between post- and predeclamping transfer
functions. The postdeclamping transfer function magnitudes were
significantly greater than the predeclamping ones for both the systolic
and the diastolic BP vs. the RRI transfer functions (repeated-measures
ANOVA, P < 0.0001). Figures 4 and 5
both demonstrate that BP affects RRI over a wide frequency range,
peaking in the 0.05- to 0.15-Hz region. This peak significantly
increased after carotid declamping. The phase lag between RRI and
systolic BP at that frequency region was between 100 and
50°, whereas the phase lag of RRI from diastolic BP was
between 180 and 120°. There were no differences
between the pre- and postdeclamping phase transfer functions. The
coherence functions of both systolic and diastolic BP vs. RRI signals
also increased significantly after declamping
(P = 0.01 and
P = 0.05, respectively), peaking in
the frequency region of 0.05-0.2 Hz.
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Fig. 4.
Mean pre- (nonbold line) and postdeclamping (bold line) transfer
functions (A) of baroreflex control
mechanism (BCM), assuming systolic (or diastolic) BP (SBP and DBP,
respectively) and RRI as input and output of system, respectively. Mean
coherence functions between systolic (and diastolic) BP and RRI are
presented in B.
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Fig. 5.
Difference between post- and predeclamping transfer function. Median
and 25th and 75th percentile functions are presented to show that
transfer function increased significantly after carotid declamping and
that increase was most significant in midfrequency region.
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DISCUSSION |
Time- and frequency-domain analysis of a system's step response is a
recognized method of studying its dynamic behavior. In the present
study, we utilized the unique conditions of carotid endarterectomy to
investigate the step baroreflex response occurring after carotid
declamping.
Two main findings emerge from our data. First, HR and BP decline after
carotid artery declamping in an exponential-like manner within
5-15 min (time constant: 6.5 ± 3.7 min) until both stabilize at the lower level. Second, carotid artery declamping causes an increase in HR and BP power spectra in their transfer function magnitude and coherence function between the two signals. The power
spectra and transfer functions increase over a wide range of
frequencies and not exclusively at the midfrequency region (0.07-0.14 Hz) commonly attributed to baroreflex activity (Figs. 3
and 4, Table 1). However, the peak increase in transfer function magnitude occurred in the midfrequency region, and no difference was
observed between the pre- and postdeclamping phase transfer functions
(Fig. 4).
Most previous studies used intravenous injection of vasoactive drugs to
trigger the BCM (18, 37). This approach is bound with major
limitations. The vasoactive drugs do not affect the baroreceptors
directly but instead alter BP by stimulating the peripheral vascular
bed and therefore directly and indirectly interfere with other elements
of the BCM. Additionally, this method induces only a short-term
disturbance in BP followed by only a brief shift in HR, a manipulation
far from being a true step input to the baroreceptors. Direct
stimulation of the carotid baroreceptors by a pneumatic neck chamber
causes a maximal change in HR within 2-4 s following a step
increase or decrease in neck pressure (4, 9, 21); yet, with this method
also, the step change in neck pressure can be maintained in humans for
only a brief period of time (<5 s; Ref. 8) for obvious reasons. Step
increase in carotid pressure in conscious healthy dogs with a
surgically isolated carotid sinus caused a decline in HR and BP within
10-20 s, with complete stabilization after 40-60 s (39). True
step baroreflex response has never been studied in humans, and no
previous study has ever shown a prolonged baroreflex response as
consistently observed in our elderly patients undergoing carotid
endarterectomy.
Figure 6 gives a schematic representation
of the main elements of the BCM, most of which are fast acting under
normal conditions. The sinoatrial (SA) node responds to carotid
stimulation within 0.5-0.6 s, and the time to peak HR change is
2-4 s (2). The latency between carotid stimulation and the
resultant diastolic BP decline is ~2.5 s, and the time to peak BP
response is 15-20 s (6, 16). Baroreceptor response time (<100
ms; Ref. 14), baroreceptor afferent nerve conduction time (~5 ms),
and vagal and sympathetic conduction time to the SA node (~55 ms) and
the peripheral vascular bed (<1 s), respectively, are all very fast (38). Nevertheless, at least three different sites in the baroreflex loop may contain longer-acting components. First, a step increase in BP
causes an immediate rise in baroreceptor nerve activity, which then
declines exponentially over the next 6-10 min by ~80% and
resets at a new lower level, even though the high BP is maintained (5).
This is known as the baroreceptors' acute adaptation mechanism (4, 26,
36). Although this mechanism alone does not explain our current
observations, it does prove the existence of slow-reacting components
in the BCM. Second, besides the SA node and arterial vascular bed, the
BCM affects also the venous vascular bed and its capacitance (10, 12).
Baroreflex sensitivity is strongly affected by cardiac preload, and
reduction in central venous pressure significantly improves the
baroreflex response in both humans and dogs (29, 32). Little is known,
however, about the time response of the venous vascular bed to
baroreflex stimulation. Previous studies on a dog model with isolated
carotid sinus and full control over arterial and venous pressures and
flows with roller pumps have shown that venous capacity and the
unstressed venous volume rise exponentially over a period of 3-6
min in response to a step increase in carotid sinus pressure
(33-35). Slowly dilating venous vessels may therefore be the
mechanism responsible for the prolonged baroreflex response observed in
patients undergoing carotid endarterectomy. Third, very little is known
about the transfer function and dynamic response of the human vasomotor center because of its complexity and inaccessibility to direct stimulation and output measurements. It is only known that the latency
period of the vasomotor center under normal conditions is
~0.2-0.4 s (8). Using an analytical model of the BCM (19, 20),
we have shown that a proportional and integrator (PI) controller included in the vasomotor center model can mimic the HR and BP time-domain behavior after carotid declamping. Moreover, an increase in
the integrator gain in the PI controller may explain the reduced baroreflex sensitivity occurring with age and in cardiovascular diseases (19). The low-pass filter effects of the PI controller may
also explain the reduced HR and BP variability in the mid- and high
frequency regions seen in elderly people with cardiovascular diseases.
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Fig. 6.
Schematic representation of BCM with its known main elements and
possible locations for proposed slowly responding components
(baroreceptors: adaptation mechanism, slow venous baroreflex response,
and proportional and integrator controller in vasomotor center). SA,
sinoatrial.
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No previous study investigated the HR and BP frequency response to a
direct step input to the carotid baroreceptors in humans. The neck
chamber technique provides a too short-term (~5 s) pulse of carotid
stimulation (1, 30), insufficient to collect adequate data for
frequency-domain analysis. As anticipated in our elderly patients
undergoing carotid endarterectomy, baseline (predeclamping) HR and BP
power spectra were markedly depressed in the mid- and high frequency
before carotid declamping. Carotid declamping "normalized" their
HR rate and BP variability as seen from the significant increase in
both HR and (systolic and diastolic) BP power spectra over the entire
frequency range (0-0.5 Hz). The transfer function, assuming BP as
an input and HR as an output, showed a maximal increase in magnitude in
the midfrequency region (~0.1 Hz), with an additional, though less
significant, increase in the high-frequency region (Fig. 4). The
coherence function between BP and HR signals, which was very low before
carotid declamping, increased after declamping and reached above the
50% level considered significant (13) in the 0.05- to 0.2-Hz region.
These findings support the concept that the midfrequency
(0.07-0.14 Hz) region in HR and BP variability is generated by the
BCM (7, 23), although other frequency regions were also affected, as
predicted on theoretical grounds by a control model of the baroreflex
loop (19, 20). Because only the amplitude and not the phase transfer
function was augmented after declamping, one may assume a nearly pure
increase in gain of the BCM after carotid declamping.
Study limitations.
We utilized the standard clinical setting of carotid surgery to study
the BCM in elderly patients with chronic cardiovascular diseases.
Although this is the strength, it is also the main limitation of the
study, restricted by the given clinical and ethical boundaries. First,
the step input was applied to only one carotid artery while the other
(carotid and aortic arch) baroreceptors remained intact and capable of
responding to the hemodynamic disturbance caused by the carotid
declamping. It is therefore possible that the mixed and multifrequency
picture obtained from the spectral analyses after carotid declamping
was in part the result of secondary reactions of the other
baroreceptors to the hemodynamic changes rather than reflecting a pure
step baroreflex response. Second, carotid artery declamping is
performed late in the surgery after the artery is dissected from its
surrounding sheath, clamped, incised, and then sutured back. It is
therefore possible that some damage to the baroreceptor nerves may have
occurred in some of the patients during the procedure. Nevertheless,
our data show that, despite the possible local damage to the
baroreceptors, there was a remarkable step increase in baroreceptor
gain after declamping as denoted by the immediate and significant
decline in both HR and BP and by the marked increase in their
variability. It is not inconceivable that the step baroreflex response
could have been even more pronounced were the baroreceptor nerves not
damaged.
In conclusion, our data obtained from elderly patients with
cardiovascular diseases undergoing carotid endarterectomy show that the
BCM may include slow-acting components which allow the cardiovascular
system to gradually adjust to abrupt changes in baroreceptor
stimulation and that the BCM is probably the generator of the
midfrequency peak in HR and BP variability, although its effect is not
limited to that region and may significantly influence other frequency
regions as well.
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FOOTNOTES |
Address for reprint requests: G. Landesberg, Dept. of
Anesthesiology and Critical Care Medicine, Hadassah University
Hospital, Jerusalem, Israel 91120.
Received 11 July 1997; accepted in final form 5 January 1998.
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Abstract
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