# Linear and nonlinear quantification of respiratory sinus arrhythmia during propofol general anesthesia.

**ABSTRACT** Quantitative evaluation of respiratory sinus arrhythmia (RSA) may provide important information in clinical practice of anesthesia and postoperative care. In this paper, we apply a point process method to assess dynamic RSA during propofol general anesthesia. Specifically, an inverse Gaussian probability distribution is used to model the heartbeat interval, whereas the instantaneous mean is identified by a linear or bilinear bivariate regression on the previous R-R intervals and respiratory measures. The estimated second-order bilinear interaction allows us to evaluate the nonlinear component of the RSA. The instantaneous RSA gain and phase can be estimated with an adaptive point process filter. The algorithm's ability to track non-stationary dynamics is demonstrated using one clinical recording. Our proposed statistical indices provide a valuable quantitative assessment of instantaneous cardiorespiratory control and heart rate variability (HRV) during general anesthesia.

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- 01/2010;
- SourceAvailable from: Luca CitiConference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 08/2011; 2011:8444-7.
- SourceAvailable from: Riccardo BarbieriIEEE transactions on bio-medical engineering 02/2010; 57(6):1335-47. · 2.15 Impact Factor

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Linear and Nonlinear Quantification of Respiratory Sinus

Arrhythmia during Propofol General Anesthesia

Z Chen, PL Purdon, ET Pierce, G Harrell, J Walsh, AF Salazar, CL Tavares, EN Brown, and R

Barbieri

Neuroscience Statistics Research Lab, Massachusetts General Hospital, Harvard Medical School,

Boston, MA, USA, Harvard-MIT Division of Health Science and Technology, and dept of Brain and

Cognitive Sciences, MIT, Cambridge, MA, USA

Abstract

Quantitative evaluation of respiratory sinus arrhythmia (RSA) may provide important information

in clinical practice of anesthesia and postoperative care. In this paper, we apply a point process

method to assess dynamic RSA during propofol general anesthesia. Specifically, an inverse Gaussian

probability distribution is used to model the heartbeat interval, whereas the instantaneous mean is

identified by a linear or bilinear bivariate regression on the previous R-R intervals and respiratory

measures. The estimated second-order bilinear interaction allows us to evaluate the nonlinear

component of the RSA. The instantaneous RSA gain and phase can be estimated with an adaptive

point process filter. The algorithm’s ability to track nonstationary dynamics is demonstrated using

one clinical recording. Our proposed statistical indices provide a valuable quantitative assessment

of instantaneous cardiorespiratory control and heart rate variability (HRV) during general anesthesia.

I. Introduction

Heart rate variability (HRV), the beat-to-beat variation in heart rate (HR), is considered to be

a reflection of autonomic nervous system activity. Respiratory sinus arrhythmia (RSA) is

thought by many to reflect the parasympathetic component of the autonomic nervous system

during spontaneous ventilation [1]. HR increases with inhalation and decreases with exhalation.

Therefore, RSA can be considered to be an important index of vagal control of HR and an

indicator of autonomic nervous system activity processed in the nucleus solitarius of the

brainstem. In clinical practice, RSA has been shown to be related to clinical signs of depth of

anesthesia and has been proposed to have potential as a diagnostic monitoring measure for the

depth of anesthesia [11],[17],[4] as well as cardiac or neurologic dysfunction [14],[13]. It was

found in animals that morphine with α-chloralose-urethane significantly increased RSA,

whereas thiopental and halothane both significantly decreased RSA [12] Studies on children

during the induction of general anesthesia with halothane and nitrous oxide showed that RSA

decreased in a significant manner, corresponding from awake, to loss of pharyngeal tone, to

stage 3 or deep anesthesia [4].

Quantitive assessment of RSA poses a challenging statistical signal processing problem in

biomedical engineering. In the literature, time domain-based sequence methods and frequency

domainbased spectral methods have been proposed to evaluate RSA [10]. However, all of these

methods are based on the assumption that signals are stationary or quasi-stationary within a

window. Previously, we have proposed a point process method to evaluate instantaneous RSA

Address for correspondence: Dr. Zhe Chen, 43 Vassar Street, Rm 46-6057, Massachusetts Institute of Technology, Cambridge, MA

02139, USA, zhechen@mit.edu.

NIH Public Access

Author Manuscript

Conf Proc IEEE Eng Med Biol Soc. Author manuscript; available in PMC 2010 January 11.

Published in final edited form as:

Conf Proc IEEE Eng Med Biol Soc. 2009 ; 1: 5336–5339. doi:10.1109/IEMBS.2009.5332693.

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during a non-stationary environment [5],[7]. Our previous investigation of RSA in a

pharmacological blockade protocol [7] validated the linear RSA gain estimates and suggested

that suppression of parasympathetic activity using atropine reduces RSA, whereas the blockade

of sympathetic activity with propranolol has little effect on the RSA gain. Here, we extend the

previous model to include a 2nd-order Volterra bilinear expansion to characterize the nonlinear

interaction between heartbeat interval and respiratory signals for a healthy subject during

general anesthesia [8] where the anesthetic drug propofol was administered with different

concentrations [18]. Our preliminary study provides a firsthand quantitative assessment of RSA

under propofol anesthesia for healthy subjects using a rigorous statistical estimation method.

II. Heartbeat Interval Point Process Model

Given a set of R-wave events

− uj−1 > 0 denote the jth R-R interval. By treating the R-waves as discrete events, we may

develop a probabilistic point process model in the continuous-time domain. Assuming history

dependence, the waiting time t − uj (as a continuous random variable) until the next R-wave

event can be modeled by an inverse Gaussian model [2],[3],[5]:

detected from the electrocardiogram (ECG), let RRj = uj

where uj denotes the previous R-wave event occurred before time t, θ > 0 denotes the shape

parameter, and μRR (t) denotes the instantaneous R-R mean. When the mean is much greater

than the variance, the inverse Gaussian can be well approximated by a Gaussian model with a

variance equal to . In point process theory, the inter-event probability p(t) is related to

the conditional intensity function (CIF) λ(t) by a one-to-one transformation:

. The estimated CIF can be used to evaluate the goodness-of-fit of the

probabilistic heartbeat model.

In modeling the instantaneous R-R interval mean μt, we propose to use the following two

models:

•

A linear bivariate autoregressive (AR) model that reflects a bivariate discrete-time

linear system:

(1)

where the first two terms represent the AR model of the past R-R intervals (RR), and

RPt − j denotes the value of the respiratory (RP) measure, which is synchronously

sampled at the beats prior to time t.

•

A nonlinear bivariate Volterra model that reflects a bivariate bilinear system:

(2)

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The above two models can be derived within the general framework of Volterra-Wiener theory

in nonlinear system identification [16].

A. Instantaneous Indices of HR and HRV

Heart rate is defined as the reciprocal of the R-R intervals. For time t measured in seconds, the

new variable r = c(t − uj)−1 (where c = 60 s/min) can be defined in beats per minute (bpm). By

the change-of-variables formula, the HR probability p (r) = p (c(t − uj)−1) is given by

, and the mean and the standard deviation of HR r can be derived [2]:

(3)

where μ̃ = c−1μRR and θ̃ = c−1θ. Essentially, the instantaneous indices of HR and HRV are

characterized by the mean μHR and standard deviation σHR, respectively.

B. Adaptive Point Porcess Filtering

Let

probabilistic model, we can recursively estimate them via adaptive point process filtering [3]:

denote the vector that contains all unknown parameters in the

where P and W denote the parameter and noise covariance matrices, respectively; and Δ=5 ms

denotes the time bin size. Diagonal noise covariance matrix W that determines the level of

parameter fluctuation at the timescale of Δ can be initialized either empirically from a random-

walk theory or estimated by a maximum likelihood estimate. Symbols and

denote the first- and second-order partial derivatives of the CIF w.r.t. ξ at time

t = kΔ, respectively. The indicator variable nk = 1 if a heart beat occurs in time ((k − 1)Δ, kΔ]

and 0 otherwise.

C. Quantification of RSA

From equations (1) or (2), we can derive the transfer function and frequency response between

RP (input) and RR (output). Since the RSA effect is frequency dependent, we propose the

following measure to quantify the RSA in the frequency domain [7]:

(4)

where f denotes the rate for the RR and RP measurements (the samples of both series are

assumed to be synchronized). With the estimated time-varying AR coefficients {ai(k)} and

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{bj(k)} at time t = kΔ, we may evaluate the dynamic frequency response of (4) at high-frequency

(HF) range (0.15–0.5 Hz, which is the range of respiration rhythm). The RSA gain,

characterized by |H12 (f)|, represents the effect of RP on heartbeat. Given the baroreflex gain,

we can estimate the cross-spectrum between RP (u) and RR (y) as (f) = H12 (f) (f). When the

coefficients {ai(t)} and {bj(t)}are iteratively updated, the point process filter produces an

assessment of instantaneous (parametric) RSA gain, as well as the cross-spectrum, at a very

fine temporal resolution and without using the window technique.

In addition, in order to characterize the nonlinear coupling between RP (u) and RR (y) in the

frequency domain, we can compute the cross-bispectrum [8]:

(5)

where

coefficients {hkl}, and the instantaneous R-R spectrum is

denotes the Fourier transform of the 2nd-order kernel

Let h(t) denote a vector that contains all of 2nd-order coefficients {hkl(t)}; in light of (5), we

may compute an instantaneous index that quantifies the fractional contribution between the

cross-spectrum and the cross-bispectrum [8]:

where |·| denotes either the norm of a vector or the modulus of a complex variable. The “≈” is

due to a Gaussian assumption used in deriving (5). A small value of ρ implies a presence of

significant (nonzero) values in {hkl} (i.e. nonlinearity), whereas a perfect linear Gaussian model

would imply ρ = 1.

III. Experimental Protocol and Setup

The present pilot study and experimental protocol was approved by the Massachusetts General

Hospital (MGH). Any subject whose medical evaluation was not classified as American

Society of Anesthesiologists Physical Status I was excluded from the study. Intravenous and

arterial lines were placed in each subject. Propofol was infused intravenously using a previously

validated computercontrolled delivery system running STANPUMP [19] connected to a

Harvard 22 syringe pump (Harvard Apparatus, Holliston, MA). Six effect-site target

concentrations (0–5 mcg/ml) were each maintained for 15 minutes respectively. Capnography,

pulse oximetry, ECG, and arterial blood pressure (BP) were recorded (at 1 kHz sampling rate)

and monitored continuously by an anesthesiologist throughout the study. Bag-mask ventilation

with 30% oxygen was administered as needed in the event of propofol-induced apnea. Since

propofol is a potent peripheral vasodilator, phenylephrine was administered intravenously to

maintain mean arterial BP within 20% of the baseline value [18]. The respiratory signals were

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simultaneously sampled and recorded at 1 kHz. The quantitative analysis of the BP and

baroreflex sensitivity has been reported elsewhere [8].

In the present study, as acquisition sessions are still ongoing, we focus on one specific subject.

Figure 1 shows representative R-R and respiratory recordings from this subject across 6 epochs.

Specifically, during the experiment, the phenylephrine was administered at around 2960 s after

the recording onset (which is at the drug effect-site target concentration of 2 mcg/ml), and it

was turned off at around 7580 s. In addition, hand ventilation started at around 3130 s and

ended at around 7555 s.

For the linear model (2), the bivariate orders p and q were fitted from 2 to 8 and the optimal

order was chosen according to the Akaike information criterion (AIC). For the bilinear model

(3), the order r = 2 was empirically chosen to avoid demanding computation burden, and the

initial hij was estimated by fitting the residual error via least-squares. After computing the CIF,

the goodness-of-fit of the probabilistic model for the heartbeat interval is evaluated with the

Kolmogorov-Smirnov (KS) test and autocorrelation independence test [2]. To assess the RSA,

we computed the frequency response (4) within the range of the respiratory frequency±0.15

Hz. For the majority of epochs, the respiratory frequency stays around 0.25~0.3 Hz, which is

also the frequency band in which the RR and BP time series achieved the maximum coherency.

Note that, since the respiratory measures are not calibrated, the RSA unit is arbitrary; however,

we still can measure the relative change in RSA as compared to the awake baseline (level 0)

for any specific subject.

IV. Results and Discussion

The main goal of this paper is to demonstrate that our proposed point process method is well

suited for analyzing data from clinical studies under general anesthesia, and that it provides a

valid model capable of tracking instantaneous HR, HRV, and RSA indices in a non-stationary

environment. The model was validated by well established goodness-of-fit tests [3].

Specifically for the considered subject, the KS plot lies almost entirely within the 95%

confidence bounds; meanwhile, the autocorrelation function has most autocorrelation lag

estimates within the 95% confidence bounds, suggesting that their transformed times are nearly

independent.

During general anesthesia, temporary interventions are required to stabilize vital signs. Clinical

interventions such as phenylephrine administration and artificial ventilation elicit important

transient responses and recurrent nonstationarities along the experiment. These kinds of

procedures, which are routine in the operating room environment, require an instantaneous

dynamic assessment such as the one we propose. More clearly, we show two explicit instances

in Fig. 2. In the top panel we are between level 0 and level 1, and at around 2010 s propofol

administration was initiated. Parallel to a sudden drop in mean RR we observe an increase in

variability accompanied by a drop in RSA. A second sharper drop (both in mean RR and RSA)

occurs 40 s later, then RSA values recover and stabilize around a lower level than without

anesthetic effect. In the second bottom panel, at around 2960 s, phenylephrine was administered

to restore blood pressure closer to baseline values. Consequently, a gradual drop in HRV is

accompanied by a more rapid drop in RSA. As values tend to stabilize, hand ventilation was

started at around 3125 s to compensate for a reduced respiration (see RP trace), eliciting a

sudden increase in HRV accompanied by a sharp decrease in RSA. Note the marked oscillatory

variations of RSA during hand ventilation, which could not have been observed with stationary

window-based estimates. Also note that even in such a highly non-stationary environment, the

overall goodness-of-fit of our model is still excellent (Fig. 3), although we also observed a

slight mismatch in tracking μRR right after certain transient effects (e.g., ventilation in Fig. 2).

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In Table I, the HR, HRV, LF/HF ratio, RSA gain, and the coherence (around respiration

frequency), time-averaged over each 15- minute propofol level, are reported. Specifically, the

time-averaged HR initially increased up to level 3 and then decreased; the time-averaged HRV

gradually decreased as the drug concentration level increased; the LF/HF ratio did not correlate

with drug level and showed a maximum during level 3 and a minimum during level 1; and the

RSA gain generally showed a decreasing trend from level 1 to level 5. It should be stressed

that these trends were not statistically significant. Furthermore, transient changes such as the

one observed in our example may significantly affect reliability of the averaged statistics within

the 15-min epochs of interest. In our case, this issue becomes even more relevant as a

consequence of the transient effects elicited by phenylephrine administration and hand

ventilation (Fig. 2).

Next, we investigate the nonlinear component of the RSA effect. Our investigation is motivated

by a previous study, which suggested that RSA fluctuations during anesthesia contain nonlinear

dynamic mechanisms [15]. Essentially, an increase/decrease of coherencevalues reflects the

increase/decrease of linear dependence in frequency domain between two time series, which

is also reflected in the cross-spectrum/cross-bispectrum ratio ρ.

In Table I, we can see that both the coherence and crossspectrum/cross-bispectrum ratio ρ show

similar mixed trends across the different drug levels, suggesting that the degree of RSA

nonlinearity is not a function of propofol drug level. It is interesting to point out that in our

previous investigation [8] we observed an increase of nonlinearity in heartbeat interval

dynamics from baseline to anesthesia, where the nonlinearity involved the bilinear interactions

between RR and systolic blood pressure (SBP) accompanied by a significant decrease in linear

coherence between these two series. This seems to suggest that the nonlinear component of

heartbeat interval dynamics during anesthesia is mainly contributed from the cardiovascular

(baroreflex) loop, whereas the linear interaction within the cardiorespiratory loop roughly

remains unchanged. It is also possible that the respiratory system indirectly influences HR by

modulating the baroreceptor and chemoreceptor input to cardiac vagal neurons. However, in

our experimental condition, it is difficult to separate the influence of SBP from the influence

of respiration on HRV.

V. Conclusion

We apply and validate a point process method for dynamic assessment of RSA during propofol

general anesthesia. The proposed point process method enables us to simultaneously estimate

instantaneous HR, HRV, cross-spectrum, and cross-bispectrum, all of which may serve as

useful noninvasive indicators in clinical practice. It should be emphasized that since the 15-

min time-averaged statistics may not give reliable estimates, our main point in this study is to

demonstrate the ability to provide instantaneous assessments of cardio-respiratory coupling

non-stationary events due to transient interventions as well as sudden changes in physiological

state that often occur in the operating room environment. Overall, our dynamic estimates

suggest that (i) RSA gradually decreases from awake baseline after administration of propofol

anesthesia, although whether the RSA gain may accurately measure efferent vagal activity is

still controversial [9]; (ii) the RSA effect is suppressed by the phenylephrine; and (iii) the

nonlinear interactions within the cardiorespiratory control remain relatively stable. It is known

that different anesthetic drugs have different impacts on autonomic control and cardiac vagal

tone [12]. Complementary to our previous study [8], it would be interesting to further

investigate the joint interactions between the cardiovascular and cardiorespiratory couplings

and their impact on HRV. Specifically, RSA is likely to be mediated by phasic withdrawal of

vagal efferent activity resulting from the mechanisms of baroreflex response to spontaneous

BP fluctuations or respiratory gating of central arterial baroreceptor and chemoreceptor afferent

inputs [20].

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To conclude, our statistical method and quantitative analysis may also serve as a potential

measure for diagnosis of a variety of cardiovascular diseases, such as hypertension, myocardial

infarction, and heart failure, all of which typically have abnormal RSA.

Acknowledgments

This work was supported by NIH Grants R01-HL084502, K25-NS05758, DP1-OD003646, and R01-DA015644.

The authors are with the Neuroscience Statistics Research Laboratory, Massachusetts General Hospital, Harvard

Medical School, Boston, MA 02114, USA. E. N. Brown is also with the Harvard-MIT Division of Health Science and

Technology and the Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge,

MA 02139, USA.

The authors thank L. Citi for assistance in preprocessing the data used in our experiment.

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17. Pomfrett CJD, Barrie JR, Healy TEJ. Respiratory sinus arrhythmia: an index of light anaesthesia.

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18. Purdon PL, Pierce ET, Bonmassar G, et al. Simultaneous electroencephalography and functional

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Fig. 1.

Selected snapshots of raw R-R and non-calibrated respiratory (RP, arbitrary unit) recordings

from one subject during 5 consecutive epochs (with gradually increasing levels of drug

concentration from 0 to 5 mcg/ml propofol).

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Fig. 2.

Two snapshot examples of dynamic tracking (using a linear model) for instantaneous HR,

HRV, and RSA (dashed, dash-dot and solid lines mark the onset time of propofol anesthesia,

phenylephrine, and ventilation, respectively). The red trace in the top panel shows the observed

R-R intervals, which overlays the μRR in blue trace.

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Fig. 3.

Goodness-of-fit tests by KS plot and autocorrelation plot. The line or dots falling within 95%

confidence bounds (dashed line) indicate a good fit of the probability model for heartbeat

intervals.

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Table I

Comparison of Mean Statistics at 6 Different Levels of Propofol Drug Concentrations.

μHR (bpm)

σHR (bpm)

μRR LF/HF

RSA gain

Coh. (HF)

ρ (HF)

level 0

61.23

3.18

0.712

16.85

0.894

0.928

level 1

61.83

2.04

0.517

27.05

0.968

0.961

level 2

64.73

2.29

0.982

19.82

0.906

0.899

level 3

66.90

1.87

0.905

12.51

0.821

0.984

level 4

63.13

2.01

0.876

15.99

0.882

0.964

level 5

61.88

1.36

0.679

10.89

0.925

0.987

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