FIGURE 24-7 Schematic representation of long-term beat-to-beat variability of the fetal heart rate ranging between 125 and 135 bpm. (Adapted with permission from Klavan M, Laver AT, Boscola MA:
Clinical concepts of fetal heart rate monitoring. Waltham, HewlettPackard, 1977.) he normal frequency of such waves is three to ive cycles per minute (Freeman, 2003).
It should be recognized that precise quantitative analysis of both short-and long-term variability presents several frustrating problems due to technical and scaling factors (Parer, 1985). hus, most clinical interpretation is based on visual analysis with subjective judgment of the smoothness or latness of the baseline. According to Freeman and associates (2003), no evidence suggests that the distinction between short-and long-term variability has clinical relevance. Similarly, the NICHD Workshop (1997) did not recommend diferentiating short-and long-term variability because in actual practice they are visually determined as a unit. The workshop panel defined baseline variability as those baseline luctuations of two cycles per minute or greater. They recommended the criteria shown in Figure 24-8 for quantification of variability. Normal beatto-beat variability was accepted to be 6 to 25 bpm.
Increased Variability. Several physiological and pathological processes can afect beat-to-beat variability. Greater variability accompanies fetal breathing and body movements (Dawes, 1981; Van Geijn, 1980). Pillai and James (1990) reported increased baseline variability with advancing gestation. Up to 30 weeks, baseline characteristics were similar during both fetal rest and activity. After 30 weeks, fetal inactivity was associated with diminished baseline variability, but fetal activity enhanced it. Last, the baseline fetal heart rate becomes more physiologically ixed (less variable) as the rate rises. This phenomenon presumably relects less cardiovascular physiological wandering as beat-to-beat intervals shorten with a higher heart rate.
Decreased Variability. A common cause of diminished beatto-beat variability is administration of analgesic drugs during labor (Chap. 25, p. 487). Various central nervous system depressant drugs can cause transient diminished beat-to-beat variability. Included are narcotics, barbiturates, phenothiazines, tranquilizers, and general anesthetics. Corticosteroids also dampen variability (Knaven, 2017). As one specific example, variability regularly diminishes within 5 to 10 minutes following intravenous meperidine administration, and the efects may last up to 60 minutes or longer (Hill, 2003; Petrie, 1993). Butorphanol given intravenously has similar efects (Schucker, 1996). And, chronically administered buprenorphine suppresses fetal heart rate and movement (Jansson, 2017).
Magnesium suate, widely used in the United States for tocolysis or management of hypertensive gravidas, is associated with diminished beat-to-beat variability. In a study of nearly 250 term gestations, magnesium sulfate administration led to decreased variability but without evidence of adverse neonatal efects (Duy, 2012). Others have echoed these findings (Hallak, 1999; Lin, 1988). With magnesium sulfate tocolysis of preterm labor, variability was also diminished in most reviewed studies (Nensi, 2014; Verdurmen, 2017).