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Expert offers tips on interpreting fetal heart rate. (Bradycardias vs. Decelerations).

SAN FRANCISCO -- The ability to distinguish between prolonged deceleration and bradycardia is vital in preventing fetal injury and death, Dr. Deborah Wing said at a meeting on antepartum and intrapartum management sponsored by the University of California, San Francisco.

"Some decelerations are quite ominous, while others are less so," said Dr. Wing of the department of obstetrics and gynecology at the University of Southern California, Los Angeles.

Prolonged deceleration is a decrease from the baseline of greater than 15 beats per minute, lasting more than 2 minutes but less than 10 minutes, she said.

A deceleration of greater than 10 minutes is considered a bradycardia. According to a 1997 study recurrent decelerations that occur with more than 50% of uterine contractions in any 20-minute segment are true signs of danger (Am. J. Obstet. Gynecol. 177[6]:1385-90, 1997).

"These are associated with fetal hypoxemia and acidosis," Dr. Wing said.

Fetal bradycardias--a fetal heart rate of less than 110 beats per minute--can stem from cardiac conduction defects, autoimmune diseases such as lupus or Sjogren's syndrome, or viral infections. Medications such as [beta]-blockers, maternal hypothermia or hypothyroidism, and chromosomal anomalies such as trisomy 21 or 18 are also associated with bradycardias. A bradycardia also may be a normal variant, however.

When the fetal heart rate is greater than 80 to 90 beats per minute and there is good variability a bradycardia may be a sign of an occiput posterior or transverse position.

Acute fetal heart rate deceleration from interruption of oxygen delivery to the fetus can stem from several causes. "In these cases you need to look for complications such as umbilical cord compression or prolapse, or maternal hypotension from lying in a supine position, placement of an epidural, or hemorrhage," she said.

Other complications that can cause deceleration are uterine rupture, placental abruption, tetanic contraction and maternal apnea.

When dealing with acute fetal heart rate deceleration, first exclude cord prolapse, uterine rupture and abruption if possible. The maternal blood pressure should be checked, and oxytocin should be discontinued. "Anything given to the mother that increases uterine activity can reduce the amount of uterine placental blood flow," Dr. Wing said at the meeting.

To change internal hemodynamic status and increase cardiac output, place the woman on her left side and administer a fluid bolus. Supplemental oxygen can be helpful. Tocolytics can minimize the reduction in the uterine placental blood flow and should be used as needed, Dr. Wing explained.

In interpreting fetal bradycardia, the obstetrician should keep in mind that it often comes with decreased fetal heart rate variability. Fetal heart rate variability is determined by the interaction between the sympathetic and parasympathetic arms of the autonomic nervous system.

"It can be influenced by fetal sleep, fetal movement, administration of medications, and fetal hypoxia," Dr. Wing commented. Congenital abnormalities, extreme prematurity and preexisting neurologic abnormality can also bring on decreased fetal heart rate variability.

Many medications are associated with decreased fetal heart rate variability Dr. Wing said. These medications include central nervous system depressants such as analgesics and narcotics like Demerol and morphine, barbiturates such as phenobarbital, and tranquilizers such as diazepam.

Parasympatholytics such as atropine and general anesthetics may also cause decreased fetal heart rate variability.
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Author:Boughton, Barbara
Publication:OB GYN News
Date:Sep 15, 2002
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