ABSTRACT

HRV can be related to changes in autonomic control. Two main sources of variability can be distinguished: respiratory sinus arrhythmia and spontaneous fluctuations mainly related to short-term blood pressure control (baroreflex). Respiratory sinus arrhythmia (Porges, 1995) is a reflection of the respiratory pattern into the HR pattern. During inspiration, vagal control to the heart is diminished (vagal gating), resulting in an increased HR, while during expiration this vagal suppression disappears, resulting in an increased HR (Porges et al., 1982; Grossman et al., 1991). According to this mechanism, and related to the relatively high frequency of normal breathing, it is believed that respiratory sinus arrhythmia is mainly vagally determined. The second source of variation is strongly related to baroreflex control and to the “eigenrhythm” of this control loop. In many cardiovascular variables, including HRV, a characteristic 10sec rhythm (0.10-Hz component) can be found that is modulated by baroreflex gain. Wesseling and Settels (1985) considered this type of variation as random fluctuations within the baroreflex. By using spectral analysis, Mulder (1992) distinguished three different frequency bands: a low-frequency area between 0.02 and 0.06 Hz; a mid-frequency band between 0.07 and 0.14 Hz; and a high-frequency band between 0.15 and 0.40 Hz. Other authors (Berntson et al., 1997) do not use the low-frequency band and indicate the (sometimes extended) mid-frequency area as the low-frequency band. Some authors (Pagani et al., 1986) consider the high-frequency area as completely vagally determined and consider the power in the low-frequency band as an index for sympathetic activity. The latter is an overly simplistic view because of the large effects of vagal control on the low frequencies.