Download Variability of Heart Rate and Regulation of Systolic Blood Pressure

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Heart Rate Variability
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Variability of heart rate and regulation of systolic blood.
pressure evaluated by fixed rate atrial pacing
Joerg Barnstedt, Kilian Tegethoff, Aninka Stellmacher, Jan H.
Baumert, Martin Dambacher*, Monika Adt and Axel W. Frey*
Deutsches Herzzentrum Berlin, Institut !%r Anaesthesiologie,
Augustenburger Platz 1, 13353 Berlin, Germany,
*Hen-Zentrum Bad Krozingen, 79188 Bad Krozingen, Germany
Introduction: In this study we investigated cardiovascular
regulation using spectral analysis of variability of heart rate (HRV)
and systolic arterial blood pressure (BPV).
It is well known that most of the autonomic regulation of
heartbeat effects on the sinus node. Using fixed rate atrial pacing,
we wanted to determine the contribution of AV-variability to total
HRV and evaluate sympathetic and parasympathetic power in the
pacing condition compared with sinus rhythm by analysing spectral
power in each frequency band. The routine implantation of
temporal atrial pacemaker electrodes after coronary artery bypass
graft (CABG) surgery allows us to obtain recordings of ECG and
invasively measured arterial blood pressure when correct function
of the external pacemaker is checked. In a former study [l], we
found that fixed rate atrial pacing reduced HRV substantially but
that there was still a residual variability detectable,which we
considered to be due to AV-variability, intrinsic cardiac circuits or
mechanical effects. The aim of this study was to review these
findings and to investigate changes in systolic blood pressure when
HRV is abolished by an external pacemaker. As variations in heart
rate are an important mechanism of autonomic cardiovascular
control, their effect on blood pressure oscillations was evaluated in
this study. The particular situation of our patients after
cardiovascular surgery was taken into account in this context.
Patients and methods: 26 patients were investigated after CABG
surgery in the operation room or.shortly after arrival on the ICU.
Patients were 43 to 76 years of age. All had normal left ventricular
function (Ejection fraction > 50%); patients with reduced renal
function, diabetes mellitus, cardiac arrhythmia and thyreotic
dysfunction were excluded from the study. No former
cardiovascular operation should have been performed on the
patients. All patients were still anaesthetized with a combination of
benzodiazepindopioidpancuronium and mechanically ventilated
with ten to twelve breaths per minute. They were medicated with
intravenous dopamine (at a dose of 10 to 30 mg per hour) and
nitrates (2.0 to 6.0 mg per hour). Electrodes of the external
pacemakers had been implanted in the right atrium at a distance of
about two centimeters from the sinus node. During recording of
data no other examinations or manoeuvers were allowed to
prevent a change in auotonomic balance induced by stress or
awakening. ECG and invasively measured arterial blood pressure
were recorded in 26 patients by copying ‘Hellige’-Monitor signals
with a portable ‘vitaport’-system. Two recordings lasting 150
seconds each were obtained from all patients. During the first
recording patients had sinus rhythm of 65 to 88 bpm. After that the
atrium was stimulated at 91 to 115 bpm. Discrete Fourier spectral
analysis was used to quantifL HRV and BPV. Power spectral
density was calculated as the area under the curve for low
fiequency spectral density (LF) between 0.003Hz and 0.15Hz and
high frequency spectral density (HF) between 0.15 Hz and 0.5 Hz.
For the determination of HRV we analysed variability of RRinterval while BPV was analysed by the determination of variability
systolic blood pressure (SBP).
Power spectra of variability during sinus rhythm were
compared with spectra during pacing in LF as well as in HF.
Median values of spectral power were compared using Wilcoxon’s
matched pairs test. A value of p < 0.05 was considered significant.
Results: Mean heart rate increases from 78-bpm to 102Xipm. HRV
decreases visibly but isn’t eliminated totally in presence of atrial
pacing:
Table 1: Changes in HRV; median values, n = 26. LF represents low
frequency, HF high frequency power spectral density (ms*/Hz)
Sinus rhythm
8.78
9.39
LF
HF
.
Pacing
0.05
1-18
HRV in the low frequencies is diminished to 99.4% of HRV
during sinus rhythm and is thus virtually abolished. In the high
frequency band the decrease of 87.4% is less distinctive than in the
low frequencies.
am
0.10
am
a+o
0.30
ay1
F K W K V CHd
Figure 1: HRV spectra during sinus rhythm (top) and pacing .
Example from one patient.
Total values of systolic and diastolic blood pressure do not
change markedly (Mean values of systolic blood pressure increase
from 127.0to 127.3mmHg while diastolic blood pressure increases
from 64.7 to 69.3 mmHg). Blood pressure fluctuations appear
during pacing in the low frequencies as well as in the high
frequencies. In fact, we observed a marked increase of HF BPV
while LF BPV changes scarcely and without any statistic
significance:
Table 2:Changes in BPV; median values, n = 26. LF represents low
frequency, HF high frequency power spectral density
fmmHe*/Hz).*D<O.OS
Sinus rhythm
Pacing
LF
2.33
2.44
HF
8 21
1 1 81
*
.
Heart Rate Variability
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FQEOUENCY I H z l
k y r e 2: Systolic BPV spectra changes during sinus rhythm (top
md pacing Example of one patient.
Discussion: It is widely accepted that low frequency fluctuations in
heart rate are mediated by the sympathetic as well as the
parasympathetic nervous system whereas. variability in frequencies
above approximately 0.15 Hz is dependent on respiration and
mediated solely by the parasympathetic system. Parasympathetic
influences preponderate over sympathetic effects in the SA node,
while there’s no dominance of sympathetic or vagal activity at the
AV node [Z]. Fluctuations in the vasomotor tone are caused by
baroceceptor feedback, thennoregulatory mechanisms [3] and local
adjustments in vascular beds [4]. They are induced by sympathetic
activity to the arterioles and conducted via the baroreflex. In the
power spectrum, oscillations in the vasomotor tone appear at
approximately 0.1 Hz [3].
The analysis of our results of low frequency and high
‘frequency changes in RR-intervals shows that LF HRV is totally
eliminated while HF HRV decreases dramatically but still exists.
Our current results are comparable to former investigations [I].
Median spectral power in the HF band is diminished to a value of
about 10% compared with sinus rhythm. This leads to the
conclusion that in the pacing condition sympathetic heart rate
variability is totally abolished. The residual variability in the high
frequencies could reveal the contribution of AV-variability to total
HRV or possibly represent an enhanced vagal tone during pacing.
Moreover, mechanical effects caused by atrial stretching or
changes in atrio-ventricular volume due to respiration, as they
occur in denervated transplanted hearts [5],must be considered to
be responsible for the detected HF HRV. All patients in our study
are mechanically ventilated with a peak inspiratory pressure of 21
to 34 mbar. As passive ventilation leads to a decrease of total HRV
with an increase of respiratory sinus arrythmia in healthy
volunteers [6], power spectral density is probably generally
reduced in our patients and the relatively high residual HF
variability may be enhanced by the passive ventilation. An
evaluation of variability of PQ-conduction time would be helpful
conduction time would be helphl for a detailed analysis of
sympathetic and parasympathetic influence on the lower conduction
system of the heart. In fact, we have co!lected such data, but as
technical inexactness in pwave detection is probably more
distinctive than PQ-variability, an exact determination is still
difficult.
The arterial blood pressure is regulated by the complex
system of baroreflex control. This control mechanism maintains
homeostasis by keeping mean blood pressure constant over short
periods and adapting it to the demand in’ longer intervals. Changes
in cardiac volume loading and cardiac output as well as changes in
the muscular tone of the peripheral vessels modulate SBP. The
elimination of HRV in our study allows us to evaluate how shortterm heart rate oscillations influence arterial blood pressure.
In the low frequencies, where arterial blood pressure
increases scarcely during pacing, BPV is caused mainly by the
variability in peripheral vasomotor activity. HRV obviously doesn’t
modulate blood pressure significantly in this frequency range. Our
findings are comparable to investigations in conscious dogs [4].
The power spectral density in the frequencies above
approximately 0.15 Hz is strongly influenced by respiration.
Changes in vasomotor tone and central venous pressure don’t have
any effect on these frequencies [7]. Our findings indicate that
normally HF oscillations in heart rate caused by respiration seem to
have a marked effect on systolic blood pressure fluctuations. We
assume that nomally HF HRV compensates HF blood pressure
fluctuations to keep arterial blood pressure as constant as possible.
Triedman et al. considered HF fluctuations in blood pressure mainly
to be caused by mechanical effects rather than autonomically
mediated mechanisms, as experiments during autonomic blockade
have shown [7]. The particular hernodynamic status of our patients
compared to a normal population must be taken into account as
well. All patients are more or less in a state of hypovolemia aRer
CABG surgery which is enhanced by treatement with intravenous
volume leads to a reduced cardiac output and therefore to a
reduced arterial pressure. We detected relatively high oscillations
in blood pressure in the low frequencies as well as in the high
frequencies which probably represent the rather instable
hemodynamic status of all patients after cardiovascular surgery.
This effect might be exaggerated by the mechanical ventilation.
During positive pressure ventilation, filling of the right heart is
reduced and thereby stroke volume and arterial blood pressure
decreases. Rooke et al. have show. that during mechanical
ventilation hemorrhage, which can also contribute in our patients
increases the variability of systolic blood pressure [8].
Conclusions: In consideration of the particular hemodynamic
status after CABG surgery we found that: HRV is detectable even
during fixed rate atrial pacing and appears only in the high
frequencies. Further investigations especially regarding the
variability of PQ-conduction time will shed light on the
physiological origin of this phenomenon. The regulation of systolic
blood pressure is strongly influenced by heart rate variations in the
respiration dependent fiequencies. Our fmdings lead to the
conclusion that HF HRV is an important regulation mechanism for
HF blood pressure fluctuations. Our results might have clinical
importance when ability of fast HR modulation is reduced, for
example in patients with congestive heart failure or permanently
implanted cardiac pacemakers.
References:
1, Tegethoff K, Baumert J-H, Frey AW,Adt M: The part of AVnode variability in total heart rate variability evaluated by fixed
rate atrial pacing. Computers in Cardiology 1994, Bethesda:
IEEE Computers Society Press:3 13-15.
2. Levy MN, Zielske H: Autonomic control of cardiac pacemaker
activity and atrioventricular conduction. J Appl Physiol 1969;
27: 447-65
Heart Rate Variability
Kitney RI: Beat by beat relationships between heart rate, blood
pressure and respiration. Kitney RI and Rompelman (Eds.): The
beat by beat investigation of cardiovascular function. Clarendon
Press Oxford 1987, 146-178
Akselrod S, Gordon D, Madwed JB,Snidman NC, Shannon C,
Cohen RJ: Hemodynamic regulation: investigation by spectral
analysis. Am. J. Physiol. 1985;246:H867-H87
Carpeggiani C. Emdin M, Balocchi et al.: Rhythmic heart rate
changes in cardiac transplantation. M. Di Rienzo et al. (Eds):
Blood pressure and heart rate variability, 10s Press, 1992:242252
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6. Haggenmiller C, Baumert JH, Adt M, Frey AW: How breathing
pattern modulates heart rate. Computers in Cardiology 1994,
Bethesda: IEEE Computers Society Press: 753-56
7. Triedman JK, Saul P: Blood pressure modulation by central
venous pressure and respiration. Buffering effects of the heart
rate reflexes. Circulation. 1994;89: 169-179
8. Rooke G.A., Schwid H. A. Shapira Y: The effect of graded
hemorrhage and intravascular volume replacement on systolic
pressure variation in humans during mechanical and spontaneous
ventilation. Anesth Analg 1995;80:925-32