Spectral and cross-spectral autoregressive analysis of cardiovascular variables in subjects with different degrees of orthostatic tolerance

Abstract

The mechanisms leading to vasovagal syncope are still unclear. A simple discriminating test for the identification of syncopeprone subjects is not presently available. Fifty-two subjects had a stepwise orthostatic test with 60 ~ tilt and -20 and -40 mm Hg lower-body negative pressure before the appearance of impending syncope symptoms. Spectral and cross-spectral analyses of heart period and systolic pressure time series were performed to estimate the power of the high-frequency (= 0.25 Hz) and low-frequency (= 0.1 Hz) oscillations, the coherence between heart period and systolic pressure, and the mean low-frequency and high-frequency central frequency, phase shift, and transfer fimction at maximal coherence. According to time to presyncope, the 52 subjects were divided into two groups: 25 with normal orthostatic tolerance, and 27 with poor orthostatic tolerance. In the supine positions, the mean central low-frequency was significantly lower in poortolerance group than in normal-tolerance group, discriminating poor from normal orthostatic tolerance with 80% specificity and 83% sensitivity, and was significantly correlated to time to presyncope. In the 2 to 3 minutes preceding syncope, subjects with poor orthostatic tolerance had less tachycardia, lower low-frequency power of systolic pressure, higher respiratory frequency, and a less negative phase shift in highfrequency range. In presyncope, sympathetic activation is reduced in subjects with poor orthostatic tolerance. In addition, the higher breathing frequency and the smaller negativity of phase shift in high-frequency range, which may indicate an inadequate engagement of the baroreflex, suggest a causal role of respiration in the development of syncope. Supine central values of low frequency may be proposed as a valuable clinical index of orthostatic intolerance. Received April 20, 2000; accepted as revised February 22, 2001Vasovagal, or neurocardiogenic, syncope is a sudden onset ofhypotension often associated with bradycardia and sometimes asystole, and leads to a short period of loss of consciousness that is usually followed by a rapid and complete recovery. Although the actual trigger mechanisms for the attack are still debated, it is now well established that there is an inappropriate change in autonomic nervous activity consisting of sympathetic withdrawal and often an increase in vagal efferent discharge [1,2]. Vasodilatation is the dominant syncope-initiating effect because prevention of bradycardia by administration of atropine or by cardiac pacing does not usually prevent the hypotension [3,4].Vasovagal attacks are associated with decreased cardiac filling and can be reproduced in a laboratory by applying a sufficiently severe orthostatic stress. Sometimes, a period of passive head-up tilting alone can induce the attacks [5], but often it is necessary to increase the stress by combining it with a vasodilator, such as isoproterenol [6] or nitrate [7], or by combining head-up tilting with suction applied to the lower body [8]. However, it may not alw...

Clinical correlates of frequency analyses of cardiovascular control after spinal cord injury

“…Although the increased cardiac baroreflex delay of ϳ1.3 s in cervical SCI subjects may seem small, it represents an increased latency of ϳ70%, which is not inconsiderable. Similar increases in latency have been seen in other pathological conditions of blood pressure regulation (21)(22)(23)(24) and in the elderly (50), in whom baroreflex responses and blood pressure control are impaired (40,41). However, the cross-spectral estimates of cardiac baroreflex function may or may not be reflected in baroreflex control of sympathetic vascular regulation.…”

“…was also less coherence in the cervical SCI group in the upright position, which may be a consequence of increased reflex delay and subsequent failure to engage the baroreflex. Interestingly, increased cardiac (21,22,24) and vascular resistance (23) baroreflex delay have been implicated in other disorders of blood pressure control and are associated with reduced coherence (22). Increased baroreflex delay is proposed to lead to instability of blood pressure homeostasis and an increased risk of orthostatic intolerance (21), a common feature in subjects with cervical SCI (10).…”

“…LF HRV is more controversial but is generally accepted to be due to oscillations in vagal outflow generated through the baroreflex and driven by sympathetically induced LF BPV (1, 2, 7, 17). Additional cross-spectral analyses of heart rate and blood pressure time series can demonstrate their interactions and assess baroreflex function (4,7,22,24) from the phase (baroreflex delay) and transfer function gain (baroreflex sensitivity) (7).…”

Cerebral autoregulation is compromised during simulated fluctuations in gravitational stress

“…Compensatory mechanisms mainly involve an increase in total peripheral vascular resistance (Brown and Hainsworth 2000) that is mediated by enhanced sympathetic outflow (Kimmerly and Shoemaker 2002;Levine et al 2002). As in other studies (Cooke et al 1999;Gulli et al 2001), we found that MAP was well maintained during the steady-state orthostatic stress, with no change in the LF power of RR-interval oscillations but with an increase in the power of LF spontaneous blood pressure oscillations. The enhanced blood pressure oscillations were not transmitted onto the cerebral circulation, indicating that autoregulation protects the cerebral vessels from sympathetically mediated perturbations in blood pressure.…”

Spontaneous Indices Are Inconsistent With Arterial Baroreflex Gain

“…Although assessing gain of a closed-loop system can be achieved by observing spontaneously occurring input and output fluctuations, the system must encompass only feedback relations, the fluctuations must be sufficiently large, and the gain must be linear across all ranges. Yet heart rate fluctuations represent both feedback and feedforward aspects of the cardiovascular system, 55 spontaneous fluctuations can at times be immeasurably small (eg, Gulli et al 56 ), and baroreflex gain is characteristically nonlinear across its range. 49 The alternative to observation is to drive the system; ie, to open the loop and observe the gain.…”