Accelerations of the human fetal heart rate at 38 to 40 weeks' gestational age

Accelerations of the human fetal heart rate at 38 to 40 weeks' gestational age

918 Correspondence August 15, 1984 Am. shock syndrome have unfolded over the last 4 years, the epidemiologic data pointed the way, 2 and the micro...

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918

Correspondence

August 15, 1984

Am.

shock syndrome have unfolded over the last 4 years, the epidemiologic data pointed the way, 2 and the microbiologic data are now defining the association. This is in the best traditions of the scientific process. The most crucial question, however, remains to be answered. Is the benefit of increased tampon absorbancy sufficient to justify the increased risk of toxic shock syndrome? Bruce A. Hanna, Ph.D. Bellevue Hospital New York University School of Medicine 560 First Avenue New York, New York 10016 Philip M. Tierno, Jr., Ph.D. University Hospital New York University School of Medicine 560 First Avenue New York, New York 10016 REFERENCES 1. Tierno PM, Hanna BA, Davis MB. Growth of toxic-shocksyndrome strain of Staphylococcus aureus after enzymic degradation of"Rely" tampon component. Lancet 1983; 1:615. 2. Hulka SS. Tampons and toxic shock syndrome. JAMA 1982;248:872.

Accelerations of the human fetal heart rate at 38 to 40 weeks' gestational age

To the Editors: The paper of Patrick, Carmichael, Chess, and Staples (AM.]. OBSTET. GYNECOL. 148:35, 1984) presents valuable information about the normal pattern of fetal heart rate accelerations near term. One of the conclusions of the authors is that a significant negative correlation exists between daily maximum amplitude of fetal heart rate accelerations and the mean daily fetal heart rate. This is in agreement with what is obtained near term by measuring the fetal heart rate response to sound stimulation' (Fig. 1). I agree with the authors that we need to modify our definitions of accelerations according to the baseline fetal heart rate. However, as can be seen from Fig. I, the intensity of the stimulus too, will influence the response. In a nonstress test, it will be difficult to compare the accelerations associated with spontaneous fetal movements, because we cannot compare the movements. In my opinion this exposes one of the limitations of the nonstress test. The authors also discuss a possible problem of recognizing fetal heart rate accelerations in the beginning of the third trimester, because of the higher baseline fetal heart rate at this gestational age. Using controlled sound stimuli, I tested the fetal heart rate response in the thirty-second, thirty-fifth, and thirty-ninth week of pregnancy 2 and found that in the thirty-second week the acceleration was not significantly correlated to the baseline fetal heart rate in contrast to the findings at later gestational ages. At least for the fetal heart rate response to sound stimulation, this suggests that at this

J. Obstet. Gynecol.

.oFHR

c beats per minute> 40

N=25

30

20

10

140 160 Prestimulation FHR (beats per minute>

Fig. 1. The relation between ~ FHR (fetal heart rate) and prestimulation FHR in 25 patients at four different stimulus

intensities. The unbroken regression lines mark the statistically significant relations for various stimulus levels. (From Jensen OH, Flottorp G. A method for controlled sound stimulation of the human fetus. Scand Audio) 11:145, 1982, with permission.)

early stage, in addition to stimulus intensity and baseline fetal heart rate level, the degree of fetal maturity also may affect the acceleration. Odd Harald jensen, M.D. Department of Obstetrics and Gynecology Akershus Central Hospital N-1474 Nordbyhagen, Norway

REFERENCES 1. Jensen OH, Flottorp G. A method for controlled sound stimulation of the human fetus. Scand Audio) 1982; 11:145.

2. Jensen OH. Fetal heart rate response to controlled sound stimuli during the third trimester of normal pregnancy. Acta Obstet Gynecol Scand 1984;63:193-7.

Reply to Jensen

To the Editors: The comments of Dr. Jensen regarding the relationship of fetal heart rate accelerations to sound stimuli are interesting. The design of studies examining the effects of sound stimulus on fetal heart rate accelerations is very difficult. Walker et al.' and Grimwade et al. 2 published two important papers on this phenomena in 1971. Their data, which measured the actual background noise in the uterus, demonstrated that the sound pressure level in decibels normally varies from 80 to approximately 50 over the sound range 20 to 200 Hz. They also demonstrated that externally applied sound is attenuated dramatically by tissues. At 100Hz the attenuation was 30 db and rose to 70 db at 5000 Hz. They concluded that the grade of attenuation