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European Journal of Heart Failure 2001 3(2):189-195; doi:10.1016/S1388-9842(00)00147-1
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© 2001 European Society of Cardiology

Altered baroreflex gain during voluntary breathing in chronic heart failure

L. Mangina,*, A. Montib, C. Médigueb, I. Macquin-Maviera, M.-E. Lopesc, P. Gueretc, A. Castaignec, B. Swynghedauwd and P. Mansierd

a Pharmacologie Clinique, Hôpital Henri Mondor Créteil, France
b INRIA-Rocquencourt Le Chesnay, France
c Fédération de Cardiologie, Hôpital Henri Mondor Créteil, France
d INSERM-U127, Hôpital Lariboisière Paris, France

* Corresponding author. Present address: Service de Pneumologie, Unité de Réanimation et Laboratoire de Physiopathologie Respiratoire, Groupe Hospitalier Pitié Salpétrière, 47–83 Boulevard de l'Hôpital, Paris 75651, France. Tel.: +33-1-42176751; fax: +33-1-42176787. E-mail address: laurence.mangin{at}psl.ap-hop-paris.fr (L. Mangin).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: We assessed the behavior of the baroreflex (BR) gain in chronic heart failure (CHF) patients using the spectral analysis method during application of a forcing stimulus, i.e. respiration.

Methods: Simultaneous RR interval and arterial pressure fluctuation recordings were obtained during two random-order periods of voluntary paced-breathing (0.15 Hz and 0.25 Hz) in seven patients with moderate CHF (NYHA class II/III; EF, 30 ± 9%; peak VO2, 18 ± 5 ml kg–1 min–1) and six age-matched controls. BR gain was assessed in the time (sequential method) and frequency (cross-spectral gain in the low and high frequency) domains.

Results: Slower breathing was associated with a BR gain decrease in CHF patients whereas a BR gain increase was evidenced in controls (BR gain: 6 ± 5 ms mmHg–1 at 0.25 Hz vs. 4 ± 3 ms mmHg–1 at 0.15 Hz, P < 0.05 in CHF; BR gain: 12 ± 7 ms mmHg–1 at 0.25 Hz vs. 15 ± 7 ms mmHg–1 at 0.15 Hz, P < 0.05 in controls).

Conclusions: Voluntary breathing, which involves cortical centers in the brain, had major effects on cardiovascular system controller gain in CHF patients, indicating an impairment of the central neural regulation of the autonomic outflow.

Key Words: Heart Failure • Respiration • Baroreflex • Autonomic nervous system • Central nervous system

Received September 15, 2000; Revised October 31, 2000; Accepted November 30, 2000


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Autonomic nervous system dysfunction is common in patients with chronic heart failure (CHF) [1]. Indexes of autonomic imbalance and neurohormonal activation add prognostic information to the left ventricular ejection fraction and predict early mortality [2–4]. Elucidation of the mechanisms underlying the genesis of autonomic dysfunction in CHF is of crucial importance since autonomic dysregulation plays a key role in progression of the disease. Heart rate modulation via low and high pressure baroreflexes is blunted in heart failure. This is ascribable to a combination of several factors, including abnormalities at the cerebral level [5,6], a shift of sympathovagal interactions towards sympathetic excitation, and alterations at several input sites in the peripheral system [7].

Various non-invasive methods based on spectral computation of transfer functions have been developed to evaluate baroreflex sensitivity. The cross-spectral ratio or gain between heart rate and blood pressure oscillations determined using a Fourier transform has been found reliable for evaluating baroreflex sensitivity [8–11]. In addition, instant spectral methods such as time–frequency analyses offer new possibilities for assessing the instantaneous response of cardiovascular oscillations to a varying breathing rate. We conducted the present study to evaluate with time and spectral methods the modulating effects of voluntary breathing on the cardiovascular system controller gain in CHF patients. Part of this work has been reported elsewhere [12].


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Patients and controls
The study included seven patients with CHF class II/III NYHA (four men and three women; mean age, 43±7 years; mean ejection fraction, 30±9%; body mass index, 27±1 kg m–2; peak O2 consumption, 18±5 ml kg–1 min–1). All were in sinus rhythm. The cause of CHF was idiopathic dilated cardiomyopathy in five patients and ischemic heart disease in two. At the time of the study, the patients had been clinically stable for at least 2 months and free of evidence of acute coronary events for at least 6 months. They remained stable with respect to therapy for at least 1 month before the study. All the patients were receiving ACE inhibitors and diuretics, five were receiving digoxin. Exclusion criteria were pulmonary disease, significant renal dysfunction, diabetes mellitus, arterial hypertension, autonomic neuropathy, and β-blocker treatment. The age- and sex-matched control group included six non-smoking, untreated, healthy volunteers (three men and three women; mean age, 42±8 years). All patients and controls gave their informed consent to participation in the study.

2.2. Experimental protocol
The recordings were performed in the morning, with the subjects lying in a darkened quiet room at 24°C. Over a period of 5 min, they were educated to pace their breathing with a periodic auditory stimulus. After a 15-min rest, the recordings were performed during two 5-min, random-order periods of breathing paced at 0.25 Hz (15 breaths min–1, which is close to the spontaneous breathing rate) and 0.15 Hz (9 breaths min–1), respectively. All seven patients were able to tolerate the slow breathing rate easily. During the paced-breathing periods, the subjects were allowed to control the depth and shape of each breath so as to preserve normal alveolar ventilation.

2.3. Measurements
During each 5-min paced-breathing period, we recorded heart rate (ECG in a lead producing a prominent R wave), blood pressure (photoplethysmographic transducer Finapress 2300, Ohmeda), and respiration (impedance method; Respitrace Systems positioned over the lower part of the chest). Non-invasive arterial blood pressure was assessed continuously with the finger kept at a constant level relative to the right atrium. This technique has been validated for power spectral analysis of arterial pressure variability [9]. The Finapress was allowed to autocalibrate during the recordings.

2.4. Data acquisition
ECG, blood pressure and respiratory signals sampled at 500 Hz were acquired on a PC computer hard disk using specific computer software (Acknowledge III, BIOPAC Systems, USA). Signal processing was performed with LARY-CVR, a physiological signal analysis software developed at the French National Institute for Research in Computer Science and Automation (INRIA) in the SCILAB-SCICOS environment. QRS complexes were detected by a derivative/adaptive threshold algorithm to provide a continuous series of RR intervals (tachogram). Systolic blood pressure detection was based on the maximal systolic value of the signal detected by an adaptive threshold (systogram) and diastolic blood pressure detection on the first minimal diastolic point detected before the maximal systolic value (diastogram). Practical implementation includes resampling of RR series, systogram, diastogram and respiratory signals at 2 Hz followed by high-pass filtering to eliminate very low frequency oscillations (≤0.04 Hz).

2.5. Spectral evaluations
Heart rate variability, blood pressure variability, and respiratory signal were first identified using a time-frequency domain method, the smoothed pseudo Wigner-Ville (SPWV) transform, which has already been used to analyse biological signals in humans [13,14]. The SPWV distribution provides a spectral profile for each beat, each depending on preceding and subsequent events, and allows time-dependent quantification of the spectral power in the low-frequency (LF) and high-frequency (HF) domains; three-dimensional spectra of RR interval, SBP, and respiratory oscillations are then produced. Details concerning these techniques have been published [13,14].

Segments were selected from the time series, i.e. the tachogram, systogram, diastogram, respiratory signal. Fast Fourier transform (FFT) was applied to a 256 Hanning window with 50% overlap. The power spectral density of the signals was computed, and the area under the spectral density curve between two limits was integrated to provide the energy in the LF and HF domains. The LF band was centered on 0.09 Hz (0.09±0.03 Hz) [15] and the HF band was centered on 0.25Hz (0.25±0.03 Hz) for recordings obtained while breathing at 0.25 Hz and on 0.15 Hz (0.15±0.03 Hz) for recordings obtained while breathing at 0.15 Hz.

2.6. Baroreflex sensitivity
In the frequency domain, cross-spectral analysis was performed to assess the coherence function between blood pressure and RR interval, with the goal of verifying that the assumption of linearity was valid. The coherence function can range from 0 to 1 and provides an estimate of the amount of linear relationship between the variabilities of the two signals at each frequency. A coherence function greater than 0.5 is required for modulus function computation. The averaged gain or spectral ratio between RR interval and blood pressure oscillations is calculated based on selected 128-s data segments. The function that describes this gain at each oscillatory frequency is the modulus of the transfer function between blood pressure and the RR interval. This technique has been described in detail elsewhere [8,11].

The spontaneous cardiac baroreflex was also evaluated in the time domain [9,16]. The method involves computer scanning of 128-s segments of the continuous finger arterial pressure recordings and ECG to locate sequences of three or more successive cardiac beats characterized by concordant (with no lag) increases or decreases in SBP and the RR interval. A linear regression between the SBP values and RR interval is applied to each of the sequences. When the correlation coefficient is greater than 0.9, the slope accurately reflects baroreflex sensitivity. The average regression slope for all sequences is then calculated to quantify baroreflex sensitivity for the 128-s data periods at each of the two breathing rates. The spectral gain and the sequential method have been validated [8–11,16].

2.7. Statistical analysis
All results are presented as means±S.D. The spectral gains were compared at the two breathing rates using non-parametric tests (Wilcoxon's test for paired comparisons and the Mann–Whitney test for unpaired comparisons). For the time-domain analysis (sequential method), the mean slopes at the two breathing rates were compared using a paired Student t-test. P values smaller than 0.05 were considered statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
3.1. Controls
Mean RR interval, systolic pressure and the standard deviation (S.D.) of the SBP signal were the same at the two breathing rates (Table 1). RR and SBP oscillations in the HF and LF domains were increased at the slower breathing rate (P<0.05, Table 1).


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  		Table 1 Heart rate variability and blood pressure variability in controls and chronic heart failure patients during voluntary paced-breathinga

 
Coherence function values between the RR interval and blood pressure oscillations were approximately 0.8–0.9, indicating a strong correlation between the two parameters (data not shown). This allowed calculation of the spectral gain. At the slower breathing rate, the baroreflex gain increased in the HF domain, denoting a frequency-dependent response (P<0.05, Table 2) whereas the BR gain remained unchanged in the LF domain.


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  		Table 2 Gain evaluated by cross-spectral analysis in controls and chronic heart failure patients during voluntary paced-breathinga

 
The sequential analysis identified 140 sequences fulfilling the above-described criteria (90 at 0.25 Hz and 50 at 0.15 Hz). The mean regression slope was higher at the slower breathing rate (10±2.8 ms/mmHg at 0.25 Hz vs. 12±2.4 ms/mmHg at 0.15 Hz, P<0.001; a typical example is shown in the top panel of Fig. 1).


Figure 01
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  		Fig. 1 Spontaneous cardiac baroreflex in the time domain in a control subject (top) and a chronic heart failure patient (bottom). In the chronic heart failure patient, the slopes are less steep at 0.25 Hz-breathing rate, as compared to controls and decrease further at 0.15 Hz.

 
3.2. CHF patients
Mean RR interval, systolic pressure and the SD of the SBP signal were similar at the two breathing rates (Table 1). HF oscillations of the RR interval and SBP were increased at the slower breathing rate (P<0.05, Table 1). As compared to controls, HF and LF oscillations of the RR interval and SBP oscillations were attenuated but showed greater depression at the slower breathing rate.

Fig. 2 shows typical three-dimensional representations of the cardiovascular and respiratory oscillations in CHF (diastolic data not shown). The HF peaks of heart rate and SBP spectra were immediately adjusted to the breathing rate (Fig. 2, RESP., RR, SBP) at 0.25 Hz and 0.15 Hz. The marked increase in the HF amplitude of SBP oscillations was accompanied by a slight increase in the HF peak of RR oscillations at the slower breathing rate.


Figure 02
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  		Fig. 2 Typical 3-D representation provided by instant time-frequency domain analysis (smoothed pseudo Wigner–Ville transform, SPWT) of respiration (RESP.), RR interval (RR), and systolic blood pressure (SBP) in a chronic heart failure patient during spontaneous breathing and paced-breathing at 0.25 Hz and 0.15 Hz. The results show persistence of respiratory modulation of autonomic outflow: at 0.15 Hz, there is a marked increase in the HF amplitude of SBP oscillations and a small increase in the HF amplitude of the RR interval oscillation underlying a frequency-dependent response of the BR gain.

 
Coherence function values between the RR interval and blood pressure oscillations in the HF and LF domains were high (data not shown), indicating that the baroreflex in the patients, although blunted, was present. Consequently, we were able to calculate the BR gain. In the CHF patients, the slower breathing rate was associated with a decrease in the gain between the RR interval and SBP in the HF domain (Table 2), whereas the opposite was seen in the controls. In the LF domain, the BR gain was unchanged.

The sequential analysis identified 100 sequences fulfilling the above-described criteria (53 at 0.25 Hz and 47 at 0.15 Hz). The mean regression slope was less steep and decreased at the slower breathing rate (5.1±1 ms/mmHg at 0.25 Hz vs. 3.5±1 ms/mmHg at 0.15 Hz, P<0.05; a typical example is shown in the bottom panel of Fig. 1).


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
The main finding of this study is that voluntary breathing in CHF patients was associated with alterations in the baroreflex gain of the cardiovascular system: slower paced-breathing decreased the BR gain in CHF whereas the opposite was evidenced in controls. The reversal of the normal pattern of breathing rate-driven BR gain change in the CHF patients suggests major dysfunction of the central neural regulation of autonomic outflow.

4.1. Central mechanisms regulating cardiovascular and respiratory rhythms
Cardiovascular rhythms are modulated by central mechanisms and afferent inputs from arterial baroreceptors, chemoreceptors, cardiac receptors, and stretch receptors in the thorax, including the lungs. During spontaneous respiration in healthy subjects, the baroreflex and cardiopulmonary reflexes are involved in the genesis of both HF and LF oscillations of heart rate and blood pressure [17]. In addition, central nervous system (CNS) has been demonstrated to play a role in the genesis of oscillatory components in cardiovascular rhythms [18–22]. Montano et al. demonstrated LF and HF components in the discharge variability of brainstem neurons recorded in anesthetized and artificially ventilated cats with sinoaortic deafferentation: an HF component synchronous with the artificial ventilation rate was evidenced in the spectrum of neuronal discharge variability [18]. Pagani et al. showed that both LF and HF of the RR interval variability are highly coherent with similar spectral components detected from the muscle sympathetic nerve activity [19]. Simultaneous changes in rhythmic organization have been evidenced in brainstem neurons, respiration, the cardiovascular system, and the EEG [20]. Voluntary breathing involves specific cortical regions in the brain that have been localized in humans [23]. The forebrain can transmit signals to the respiratory system along an independent pathway, bypassing the automatic metabolic control center (spontaneous breathing) in the brainstem [24]. Furthermore, robust connections exist between the cerebral cortex, the brainstem respiratory motoneurons, and the hypothalamic area [25,26], a cardiovascular and respiratory integrative structure. In healthy subjects, high frequency BR gain is enhanced when the breathing rate is slowed-down, i.e. there is an inverse relation between the baroreflex sensitivity and the respiratory rate [27]. Greater tidal volume causes higher cardiac output and SBP oscillations, therefore justifying the increase of the BR gain to buffer such oscillations. During voluntary breathing, the CNS also contributes to regulate the peripheral BR controller gain [26].

4.2. Altered central nervous system processing in CHF patients
Autonomic modulation of cardiovascular variabilities in CHF is characterized by alterations at the cerebral level [5,6], sympathetic excitation and vagal withdrawal [1], and profound neurohormonal derangements [4]. Arterial and cardiopulmonary baroreflex are also blunted and CNS abnormalities play a major role in the impaired regulation of autonomic outflow in CHF patients [5,6,21,22]. However, the origin of these CNS alterations remains complex. Major changes in specific cerebral areas including alterations in neuron activation occur, probably as a result of exaggerated sympathetic outflow [5]. Excessive circulating levels of catecholamines, angiotensin, or vasopressin may alter autonomic regulatory function at the central level as well [5,6]. It should be borne in mind that the patients studied were not severe, as indicated by the clinical data and the preservation of LF RR interval oscillations [22]. Consistent with this fact, respiratory modulation of the baroreflex sensitivity was preserved. In CHF, voluntary breathing has major effects on the controller gain of the cardiovascular system This novel finding reinforce the notion of a central impairment regulating autonomic outflow: using an instant non-linear time-domain method, i.e. the complex demodulation technique, we previously evidenced major phase fluctuations between cardiovascular oscillations and respiration during volitional paced-breathing, indicating transient lack of synchronization between these physiological signals [28].

Various methods for baroreflex assessment as the phenylephrine method, the {alpha}-index method in the LF and HF domains, and sequential methods have been used to measure baroreflex sensitivity in CHF patients. Although neither the phenylephrine method nor spectral analysis is ideal, the spectral gain and the sequential methods have the enormous advantage of being non-invasive for the patients. [29,30].

4.3. Study limitations
One limitation of our study is that tidal volume was not measured and therefore we can not exclude that differences in tidal volume may alter pulmonary stretch receptors inputs differentially in normal vs. heart failure. However the central impairment in CHF that we evidenced during volitional breathing play the major role in the reversal of gain. Another possible limitation is that we didn't measure blood gases during the controlled-breathing period and chemoreflexes have direct effects on the baroreflex function. However tidal volume was not controlled to preserve normal alveolar ventilation in order to minimize blood gases changes.


   References
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 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

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