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Maternal Hypothermia and Persistent Fetal Bradycardia During the Intrapartum Process
Maternal Hypothermia and Persistent Fetal Bradycardia During the Intrapartum Process Melanie J. Reis, RN, MN, Helene White Dodson, RN, BSN
Maternal hypothermia can be correlated with persistent fetal bradycardia. The improvement of the maternal hypothermic state and the subsequent alleviation of fetal bradycardia are presented in two case reports. A possible consequence of unrelieved maternal hypothermia at delivery, neonatal cold stress, is discussed in a third case report. Neonatal complications requiring interventions may ensue after cold stress.JOGNN, 25, 674-680; 1996.
Accepted: April 1995
clothing, evaporation from the skin in a cool environment, inability or decreased ability to shiver, decreased metabolic rate, and aging (Thompson et al., 1993). Fetal bradycardia is a baseline fetal heart rate (FHR) of less than 120 bpm, or a drop of at least 30 bpm from the baseline for a duration of 10 minutes or longer (Freeman & Garite, 1981; Tucker, 1992; West, Chez, & Miller, 1993). There are several known reasons for fetal bradycardia. These include late (profound) fetal hypoxia, maternal hypotension, medications or drugs (i.e., "caine" drugs used for paracervical blocks and beta blockers), bradyarrhythmia, prolonged umbilical cord compression, postterm delivery, connective tissue disease (e.g., lupus), maternal hypothermia (Cabaniss, 1993; Freeman & Garite, 1981; Martin, 1990; Murray, 1988; Olds, London, & Ladewig, 1992; Tucker, 1992; West et al., 1993), maternal cardiopulmonary bypass procedures with a nonpulsatile blood flow o a d h o n & Main, 1988; Johnson & Saltzman, 1991), and occiput posterior position (Cabaniss, 1993; Gimovsky & Caritis, 1982).
a large southeastern tertiary perinatal center, ersistent fetal bradycardia (105-1 15 beats per minute [bpm]) was noted on the fetal monitor tracing of a laboring client who was at low risk. The external fetal monitor tracing was reassuring, with long-term variability (LW) present and several spontaneous accelerations of 20-30 bpm above the baseline. The mother's temperature at admission was 95.8"F (35.5"C) (see Case Report 1). Several other cases of persistent fetal bradycardia occurred in this perinatal center, and, again, they were associated with maternal hypothermia. The physicians and nursing staff were unable to find a cause for the maternal hypothermia. The clients' histories were all negative for any known causes of maternal hypothermia. Maternal hypothermia in the laboring woman is an oral temperature of less than 97.6"F (36.5"C) (Martin, 1990). Several known causes for maternal hypothermia have been reported. These include sepsis, magnesium sulfate infusion, operative-induced hypothermia (cardiac and neurosurgical procedures), cold environment, physical illness (i.e., hypothyroidism), and hypoglycemic shock (Cabaniss, 1993;Jadhon &Main, 1988;Rodis, Vintzileos, Campbell, Deaton, & Nochimson, 1987; Thompson, McFarland, Hirsh, & Tucker, 1993). Hypothermia also has been associated with inactivity, medications causing vasoconstriction, trauma, wet or inadequate
Medical and nursing literature reviews noted few references to either maternal hypothermia in labor or its association with fetal bradycardia. Four reports were found associating maternal hypothermia with fetal bradycardia. Jadhon and Main (1988) reported a case of urosepsis with maternal hypothermia and an associated fetal bradycardia. A second report by Rodis et al. (1987) involved magnesium sulfate infusion for premature onset of labor that resulted in maternal hypothermia and fetal bradycardia.
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Even though this decreased fetal baseline without signs of distress is considered benign, a potential risk to the newborn from hypothermia caused concern.
Maternal Hypothermia and Fetal Bradycardia
Figure 1. Internalfetal monitor tracingfor Cave 1, a 22-year-oldwoman,gravida I.para 0, at 40 weeks gestation with spontaneow. rupture ofmembranes at 1:OO a.m.
Two case reports by Cabaniss (1993) linked fetal bradycardia and maternal hypothermia. One involved severe insulin shock, and the other occurred after treatment with antibiotics for pyelonephritis of a client with known adrenocorticotropic deficiency and hypothyroidism. Maternal hypothermia was mentioned by several authors as a cause of fetal bradycardia (Freeman & Garite, 1981; Martin, 1990; Murray, 1988; Olds et al., 1992; Tucker, 1992; West et al., 1993). Maternal (and therefore fetal) hypothermia reduces myocardial metabolism, decreases oxygen requirements, and decreases the heart rate (Martin, 1990; Tucker, 1992). Fetal bradycardia with no change in a previously reassuring fetal monitor tracing is not considered to be a sign of fetal distress and can be classified
10C
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-k
98
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97
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-Maternal Temperature -.+.-Fetalheartrate
A
e!
!i
95
.
....... ......
94 0300 0500 0700 0800 0900 I000 1200
Time
Figure 2. Maternal temperature andfetal heart ratefor Case 1.
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as benign (Tucker, 1992). Even though this decreased fetal baseline without signs of distress is considered benign, a potential risk to the newborn from hypothermia is a cause for concern.
Assessment of Fetal Heart Rate Tracings Assessment of the FHR tracing must be made individually for each fetus. The final interpretation of the FHR pattern falls into either the category of reassuring or nonreassuring. Three factors must be considered in this assessment. They are the FHR, variability assessment, and the occurrence of FHR changes-periodic and nonperiodic deviations (Murray, 1988; Tucker, 1992; West et al., 1993). Determining the FHR baseline is the initial step in this assessment. The normal baseline is between 120 and 160 bpm. Fetal bradycardia or tachycardia alone does not necessarily indicate fetal distress (West et al., 1993). After the FHR baseline is determined, variability of the tracing is evaluated. A reassuring fetal monitor tracing shows fluctuations of the FHR baseline that are described as variability. Long-term variability is the waviness of the FHR tracing assessed over time and can be observed with external and internal fetal monitoring. Short-term variability (STV) is the “push-pull” effect of sympathetic and parasympathetic nervous system input and can be assessed only with a spiral electrode (Freeman & Garite, 1981; Martin, 1990; Murray, 1988; Olds et al., 1992; Tucker, 1992; West et al., 1993). Freeman and Garite (1981), Murray (1988), and Petrie (1991) state that variability is the most important characteristic of the FHR in predicting the status of a fetus. Normal variability should be observed after 28 weeks gestation (Petrie, 1991). The presence of normal variability is one of the best indicators of an intact pathway between the central nervous system and the heart (Murray, 1988; Petrie, 1991).
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**,I#
...
..,
(1
I S
..t UI
Figure 3. ExternulJetul monitor tracingfor Case 2, u 311vear-oldwomun. gruvidu 11.paru I, at 36 weeks gestution. with premature rupture of memhrunes at 1250 a.m.
Finally, an assessment is made of accelerations and decelerations. A reassuring tracing indicates the presence of spontaneous accelerations and absence of late decelerations (West et al., 1993). Fetal bradycardia with the presence of such reassuring features as average variability and/or spontaneous accelerations indicates that a fetus is under a degree of stress but has enough oxygen and metabolic reserve to compensate (West et al., 1993). Fetal bradycardia accompanied by average variability is only a stressful incident and usually well tolerated by the fetus (Cabaniss, 1993; Gimovsky & Caritis, 1982; West et al., 1993). However, fetal bradycardia without such variability represents direct myocardial depression. This is a nonreassuring pat-
tern requiring immediate intervention (Gimovsky & Caritis, 1982; West et al., 1993). In our center, we observe for reassuring tracings using the external fetal monitor. When a nonreassuring tracing is noted, we consider using a spiral electrode and obtaining a scalp pH.
Interventionsfor Maternal Hypotbermk Three reports of persistent fetal bradycardia associated with maternal hypothermia in laboring clients are presented for review (see Cases 1, 2, and 3). The presence of L T V and STV remained constant in each episode reported. Initially, all three patients received the routine care provided to all laboring clients. They were assessed
~~
Figure 4 Externalfetal monitor tracingfor Case 2 at 8 55 a m Sterile vaginal examination showed 7 cm drlatation/ 80%effuced/O station
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Maternal Hypothermia and Fetal Bradycardia
in the labor and delivery triage area and then moved to an adjacent labor, delivery, and recovery room. Several different labor, delivery, and recovery rooms were used for these clients. The women were infused with room temperature intravenous solutions of lactated Ringer's or dextrose 5% lactated Ringer's solution. These three episodes were observed in heated and air-conditioned rooms. During discussions with other nursing staff members, it was mentioned that a retired nurse with many years o f labor and delivery experience had noted the correlation between fetal bradycardia and maternal hypothermia. Because this association was not common knowledge among our physicians or nursing staff, steps to correct maternal hypothermia were not implemented routinely.
100
150 -Maternal
/!-
Temperature
99 -
-e
98
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97
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E
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..*..Fetal heart rate
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-al 110 g U S
96100 95
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944
80 0100
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Figure 5 Muternal temperutureand,fitul heart ratejbr Cave 2.
Because of the potential for metabolic complications, a neonate experiencing cold stress may need to be assessed as frequently as every 15-30 minutes during the initial neonatal period.
As this correlation became more evident, the nursing staff and physicians intervened to increase the temperature of the mothers. Nursing measures included using warm fluids, warm blankets, stockinette caps, and socks. Intravenous fluids and blankets are stocked in warming cabinets in our unit. If further interventions were warranted, the nursing staff obtained a physician's order for a fluid warmer and/or a thermo-controlled blanket, which were used to produce successful results. In most cases, the mother's temperature began to rise. It was observed that the fetal bradycardia abated as the maternal temperature increased. The rectal temperature of the neonate also was within normal limits, except in Case 3, in which the maternal hypothermia was not resolved fully by delivery. In that case, the maternal temperature at delivery was 95.6"F ( 3 5 3 ° C ) degrees and the neonate's initial temperature was 96.0°F (35.6"C) degrees. The normal range for rectal temperature in a neonate is 97.8"F99.O"F (36.6"C-37.3"C) (Olds et al., 1992). This subnormal temperature can lead to neonatal cold stress.
Neonatal Risks Neonatal cold stress is an excessive heat loss that results in compensatory mechanisms being used to maintain core body temperature. The metabolic consequences of cold stress can be devastating and are potentially fatal to the infant (Olds et al., 1992). Because of the potential for complications, a neonate who experiences cold stress
October 1996
may need to remain in a thermo-controlled environment for several hours; rapid warming of the neonate can lead to apnea (Olds et al., 1992). Interventions during this initial neonatal period may include an evaluation for hypoglycemia and skin temperature assessments as frequently as every 15-30 minutes. This could interfere with newborn-family attachment. Parents can be present in the nursery while the neonate is under a radiant warmer, but such a situation is not ideal for the initial hours after delivery.
Nursing Implications Determination of the cause of persistent fetal bradycardia (as is done with fetal tachycardia) can help to establish the need for interventions. An investigation is recommended when persistent fetal bradycardia is noted (Cabaniss, 1993; Roberts, 1989). Assessment of the maternal temperature by either a tympanic or axillary mode may be more reliable than orally when oxygen is in use or ice chips or popsicles are being consumed. Perinatal standards of the American College of Obstetrics and Gynecologists call for assessing the mother's temperature every 4 hours during the intrapartum period (Freeman & Poland, 1992). When the membranes rupture, the mother's temperature should be assessed every 1-2 hours (Martin, 1990; Olds et al., 1992;West et al., 1993). If the cause of persistent fetal bradycardia is determined to be maternal hypothermia with n o attributable factors, nursing and medical interventions to increase the maternal temperature may be required before there is an alleviation of the fetal bradycardia. Maternal temperature assessments may be required hourly until resolution of the variance. A side effect of maternal hypothermia may be a slowing of the labor progress, as noted in Cases 1 and 3, when the transition phase lasted 3% hours and 4 hours, respectively. Observing for a correlation between fetal bradycardia and maternal hypothermia may assist the nurse in evaluating the fetus during the second stage of labor. If fetal bradycardia
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Figure 6. Exlernulfeul monitor Irucingjbr Cuse 3 a1630 a.m. S l e d e vaginal exminulion sbowed 4-cm dilutalion/ 100%eJaced/- 1 stufion.
persists into the second stage of labor, the presence of variable decelerations may concern the caregivers. When a deceleration occurs from an already significant low baseline, the fetus may not receive adequate perfusion of vital structures during the deceleration. In this instance, the caregiver would expect to find evidence of progressive development of hypoxic changes (Cabaniss, 1993).
Sum ma ry Using astute observation and the correlation between maternal hypothermia and fetal bradycardia, labor and delivery nurses can initiate appropriate interventions. Early interventions to correct the maternal hypothermic state before delivery can avoid possible neonatal problems. Preventing a state of newborn hypothermia, which can lead to problems for the neonate from cold stress, is a desired goal for perinatal nurses.
Case I A 22-year-oldgravida I, para 0, at 40 weeks gestation with spontaneous rupture of the membranes occurring at 1 a.m. was admitted to labor and delivery at 3:30 a.m. with
early labor (3-cm dilatation). Her vital signs at admission were blood pressure, 129/87; temperature, 95.8" F
Early interventions to correct the maternal hypothermic state before delivery can avoid possible neonatal problems.
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(35.5"C); pulse rate, 94; and respiration rate, 20. The FHR baseline was 105-115 bpm with a reassuring tracing on an external fetal monitor. The mother's physician and nurse were unable to ascertain a cause of the maternal hypothermia. Results were negative from blood tests ordered to rule out sepsis. Because it was winter, a social assessment was performed and the mother's home was noted to have heat. One milligram of butorphanol tartrate was given intravenously at 4:15 a.m. for labor pain, and epidural anesthesia was begun at 4 5 0 a.m. Her vital signs remained stable, with a temperature of 9 6 . 7 " (36.0"C) ~ and FHR of 90-1 10 bpm. A spiral electrode was placed on the scalp of the fetus at this time. Average LTV remained and STV was present (see Figure 1). At 6:15 a.m., the mother's cervical dilatation was 8 cm with 100% effacement. At 7:OO a.m., her temperature decreased to 95.6"F (35.3"C). Warm blankets, a stockinette cap, intravenous fluids via a fluid-warmer, and a thermo-controlblanket were used to conserve and increase the mother's body heat. A simultaneous increase in maternal temperature and FHR baseline was noted at 8:OO a.m. Slow cervical dilatation progressed. Pushing was initiated at 1O:OO a.m. when the cervix was dilated completely and the fetal head was at +1 station. The FHR baseline was now 115125 bpm, and the maternal temperature increased to 9 8 9 ° F (37.2"C). A viable boy was born 2 hours and 30 minutes later with Apgar scores of 6 and 8 at 1 and 5 minutes, respectively. The maternal temperature at delivery was 98.4' F (36.9"C), and the neonate's initial temperature was 99.1"F (37.3"C). This case shows how the correction of maternal hypothermia correlated with the correction of fetal bradycardia. The outcome of the neonate's core temperature was favorable.
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Maternal Hypothermta and Fetal Bradycardia
Figure 7. lnternul~talmonitor tracing and internal uterine pressure catheterjor Case 3 at 1050 a.m.
Case2 A 31-year-oldgravida 11,para I, at 36 weeks gestation with premature rupture of membranes, presented to the labor and delivery unit in early labor. At 12:46 a.m., her vital
signs at admission were blood pressure, 129/74; temperature, 98.7"F (37.0"C); pulse rate, 71; and respiration rate, 18. The FHR baseline was 130-140 bpm on an external fetal monitor, with a reassuring tracing (see Figure 3). An intravenous oxytocin infusion was begun. Ninety minutes later, the maternal temperature was 97.7"F (36.5"C) and the FHR baseline was 120-130 bpm. The maternal temperature continued to decrease during the next several hours, and the FHR baseline decreased simultaneously. A reassuring tracing continued to be present. Neither the nursing staff nor physician were able to
0..
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-Maternal
Temperature
. .+. . Fetal heart rate
99 -
- 130 - 120
t f
-
-
I
'B
97-
110
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94 0600
0700
0900
1100
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Figure 8. Muternal temperature andfetal heart rate trucingfor Case 3.
October 1996
Case3
g e
A 26-year-old gravida 11, para I, at 39 weeks gestation was admitted to the labor and delivery unit in active labor (4-
1
cm dilatation). Her admitting vital signs were blood pressure, 130/72; temperature, 98.4"F (36.9"C); pulse rate, 83; and respiration rate, 20. The FHR baseline was 130140 bpm, with a reassuring fetal monitor tracing on an external fetal monitor (see Figure 6). Two hours later, the maternal temperature decreased to 96.4"F (35.8"C) and the FHR baseline was 110-125 bpm with minimal LTV. The transition phase began at 8:OO a.m. At 10:05 a m . , an intrauterine pressure catheter and a spiral electrode were placed by the physician. The maternal temperature continued to decrease, which concerned the
I 100 =
-90
diagnose a cause for this decrease in the maternal temperature. Intravenous butorphanol tartrate was given to the mother for pain at 3:30 a.m. At 7:OO a m . , an amnioinfusion for variable decelerations was begun via a fluid warmer per our unit protocol. A fetal scalp pH test performed at 8:50 a.m. was 7.31. At 9 0 0 a m . , the maternal temperature remained low at 95.6"F (35.3"C), with the FHR baseline at 100-110 bpm (see Figure 4). A thermocontrol blanket, another medical intervention, was applied at this time. A resulting increase in the maternal temperature to 97.8"F (36.6'C) was noted 1 hour later. The FHR baseline increased to 112-118 bpm. The thermo-control blanket was discontinued. During the next hour, the maternal temperature and FHR baseline returned to the admission range. Apgar scores for the neonate were 8 at 1 minute and 9 at 5 minutes. The neonate's initial temperature was 97.4"F (36.5"C).After correlating the decrease in the FHR baseline with maternal hypothermia, interventions were initiated, and again, a favorable outcome in terms of neonatal core temperature was obtained.
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physician and nursing staff. Three hours into the transition phase, the maternal temperature was 95.4' F (35.2"C),and the FHR was 95-110 bpm, with STVpresent (see Figure 7). Hydration with warm intravenous fluids began at 1O:OO a.m. for epidural anesthesia. N o relief was noted from the maternal hypothermia, and, therefore, the physician ordered a thermo-control blanket. At 10:30a m . , pushing began because cervical dilatation was complete and the fetal head was at +1 station. N o change in the maternal temperature or FHR was noted. Early decelerations with a decrease in the FHR down to 60 bpm were noted during the second stage of labor. A viable boy with Apgar scores of 6 and 8 was delivered after 30 minutes of pushing. The mother's initial temperature postpartum was 9523°F (35.5"C), and the neonate's initial temperature was 96.O"F (35.7"C). The neonate was placed under an infant warmer in the extended-care nursery. The neonate's temperature slowly increased to 98.O"F (36.7"C) 90 minutes after delivery. During this period, skin assessments every 15 minutes were required. Warm blankets were placed on the mother, and her temperature increased to 98.O"F (36.7"C) within 2 hours. This case shows the possible result when the correlation between maternal hypotherrnia and fetal bradycardia remains undiagnosed or when interventions are not initiated expediently. Although no complications developed, the potential for neonatal cold stress was present.
References
(Ed.), Anesthetic & obstetric management of high-risk pregnancy (pp. 210-259). St. Louis: Mosby-Year Book. Martin, E. J. (1990). Admission assessment of the laboring woman. In S. M. Glover (Ed.), Intrapartum Management Models: A Perinatal Education Program (pp. 59-98). Baltimore: Williams (G Wilkins. Murray, M. (1988). Antepartum a n d intrapartalfetal monitoring. Baltimore: Williams & Wilkins. Olds, S., London, M., Lk Ladewig, P. (1992). Maternal-Newborn Nursing (4th ed.). Redwood City: Addison-Wesley Nursing. Petrie, R. H. (1991). Intrapartum fetal evaluation. In S. G. Gabbe, J. R. Niebyl, & J. L. Simpson, (Eds.), Obstetrics: Normal &problem pregnancies (2nd ed., pp. 457-491). New York: Churchill Livingstone. Roberts, J. E. (1989). Managing fetal bradycardia during second stage of labor. MCN: American Journal of Maternal/Child Nursing, 14, 394-398. Rodis, J. F., Vintzileos, A. M., Campbell, W. A., Deaton, J. L., & Nochimson, D. J. (1987). Maternal hypothermia: An unusual complication of magnesium sulfate therapy. American Journal Obstetrics a n d Gynecology, 156(2), 435-436. Thompson, J., McFarland, G., Hirsch, J., & Tucker, S. (1993). Health perception-health management. In S. Schrefer (Ed.), Mosby's clinical nursing (pp. 1470-1473). St. Louis: Mosby-Year Book Tucker, S. (1992). Baseline fetal heart rate. In T. V. Schaik (Ed.), Pocket guide to fetal monitoring (2nd ed., pp. 65-82). St. Louis: C.V. Mosby Co. West, J., Chez, B. F., & Miller, F. C . (1993). Fetal heart rate. In R.A. Knuppel & J.E. Drukker, (Eds.), High riskpregnancy, a team approach (2nd ed., pp. 316-336). Philadelphia: W.B. Saunders.
Cabaniss, M. L. (1993). Fetal monitoring interpretation. Philadelphia: J.B. Lippincott. Freeman, R. K., (G Garite, T. J. (1981). Baseline shifts. In Fetal heart rate monitoring (pp. 63-68). Baltimore: Williams & Wilkins. Freeman, R. K., & Poland, R. L. (Eds.). (1992). Guidelines for perinatal care (3rd ed.) Elk Grove Village, IL: American Academy of Pediatrics. Gimovsky, M. L., & Caritis, S. N. (1982). Diagnosis and management of hypoxic FHR patterns. Clinics in Perinatology, H 2 ) , 313-324. Jadhon, M., 62 Main, E. (1988). Fetal bradycardia associated with maternal hypothermia. Obstetrics a n d Gynecology, 72(3), 496-497. Johnson, M., (G Saltzman, D. (1991). Cardiac disease. In S. Datta
Helene White Dodson is a staff nurse andpreceptor in Labor and Deltveryptgh-Risk Obstetric Care at Arnold Palmer Hospitalfor Chtldren G Women in Orlando, FL.
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Addressfor correspondence: Melanie J. Rets, RN, MN, CNS, Arnold Palmer Hospttal f o r Children G Women, Labor and Delivery MP 321,92 W.Miller St., Orlando, FL 32806. Melante J. Reis is a pertnatal clinical nurse specialist in Outcomes Management at Arnold Palmer Hospital f o r Chtldren G Women in Orlando, FL.
Maternal hypothermia can be correlated with persistent fetal bradycardia. The improvement of the maternal hypothermic state and the subsequent alleviation of fetal bradycardia are presented in two case reports. A possible consequence of unrelieved maternal hypothermia at delivery, neonatal cold stress, is discussed in a third case report. Neonatal complications requiring interventions may ensue after cold stress.JOGNN, 25, 674-680; 1996.
Accepted: April 1995
clothing, evaporation from the skin in a cool environment, inability or decreased ability to shiver, decreased metabolic rate, and aging (Thompson et al., 1993). Fetal bradycardia is a baseline fetal heart rate (FHR) of less than 120 bpm, or a drop of at least 30 bpm from the baseline for a duration of 10 minutes or longer (Freeman & Garite, 1981; Tucker, 1992; West, Chez, & Miller, 1993). There are several known reasons for fetal bradycardia. These include late (profound) fetal hypoxia, maternal hypotension, medications or drugs (i.e., "caine" drugs used for paracervical blocks and beta blockers), bradyarrhythmia, prolonged umbilical cord compression, postterm delivery, connective tissue disease (e.g., lupus), maternal hypothermia (Cabaniss, 1993; Freeman & Garite, 1981; Martin, 1990; Murray, 1988; Olds, London, & Ladewig, 1992; Tucker, 1992; West et al., 1993), maternal cardiopulmonary bypass procedures with a nonpulsatile blood flow o a d h o n & Main, 1988; Johnson & Saltzman, 1991), and occiput posterior position (Cabaniss, 1993; Gimovsky & Caritis, 1982).
a large southeastern tertiary perinatal center, ersistent fetal bradycardia (105-1 15 beats per minute [bpm]) was noted on the fetal monitor tracing of a laboring client who was at low risk. The external fetal monitor tracing was reassuring, with long-term variability (LW) present and several spontaneous accelerations of 20-30 bpm above the baseline. The mother's temperature at admission was 95.8"F (35.5"C) (see Case Report 1). Several other cases of persistent fetal bradycardia occurred in this perinatal center, and, again, they were associated with maternal hypothermia. The physicians and nursing staff were unable to find a cause for the maternal hypothermia. The clients' histories were all negative for any known causes of maternal hypothermia. Maternal hypothermia in the laboring woman is an oral temperature of less than 97.6"F (36.5"C) (Martin, 1990). Several known causes for maternal hypothermia have been reported. These include sepsis, magnesium sulfate infusion, operative-induced hypothermia (cardiac and neurosurgical procedures), cold environment, physical illness (i.e., hypothyroidism), and hypoglycemic shock (Cabaniss, 1993;Jadhon &Main, 1988;Rodis, Vintzileos, Campbell, Deaton, & Nochimson, 1987; Thompson, McFarland, Hirsh, & Tucker, 1993). Hypothermia also has been associated with inactivity, medications causing vasoconstriction, trauma, wet or inadequate
Medical and nursing literature reviews noted few references to either maternal hypothermia in labor or its association with fetal bradycardia. Four reports were found associating maternal hypothermia with fetal bradycardia. Jadhon and Main (1988) reported a case of urosepsis with maternal hypothermia and an associated fetal bradycardia. A second report by Rodis et al. (1987) involved magnesium sulfate infusion for premature onset of labor that resulted in maternal hypothermia and fetal bradycardia.
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Even though this decreased fetal baseline without signs of distress is considered benign, a potential risk to the newborn from hypothermia caused concern.
Maternal Hypothermia and Fetal Bradycardia
Figure 1. Internalfetal monitor tracingfor Cave 1, a 22-year-oldwoman,gravida I.para 0, at 40 weeks gestation with spontaneow. rupture ofmembranes at 1:OO a.m.
Two case reports by Cabaniss (1993) linked fetal bradycardia and maternal hypothermia. One involved severe insulin shock, and the other occurred after treatment with antibiotics for pyelonephritis of a client with known adrenocorticotropic deficiency and hypothyroidism. Maternal hypothermia was mentioned by several authors as a cause of fetal bradycardia (Freeman & Garite, 1981; Martin, 1990; Murray, 1988; Olds et al., 1992; Tucker, 1992; West et al., 1993). Maternal (and therefore fetal) hypothermia reduces myocardial metabolism, decreases oxygen requirements, and decreases the heart rate (Martin, 1990; Tucker, 1992). Fetal bradycardia with no change in a previously reassuring fetal monitor tracing is not considered to be a sign of fetal distress and can be classified
10C
99
-k
98
@
97
L
6
-Maternal Temperature -.+.-Fetalheartrate
A
e!
!i
95
.
....... ......
94 0300 0500 0700 0800 0900 I000 1200
Time
Figure 2. Maternal temperature andfetal heart ratefor Case 1.
October 1336
as benign (Tucker, 1992). Even though this decreased fetal baseline without signs of distress is considered benign, a potential risk to the newborn from hypothermia is a cause for concern.
Assessment of Fetal Heart Rate Tracings Assessment of the FHR tracing must be made individually for each fetus. The final interpretation of the FHR pattern falls into either the category of reassuring or nonreassuring. Three factors must be considered in this assessment. They are the FHR, variability assessment, and the occurrence of FHR changes-periodic and nonperiodic deviations (Murray, 1988; Tucker, 1992; West et al., 1993). Determining the FHR baseline is the initial step in this assessment. The normal baseline is between 120 and 160 bpm. Fetal bradycardia or tachycardia alone does not necessarily indicate fetal distress (West et al., 1993). After the FHR baseline is determined, variability of the tracing is evaluated. A reassuring fetal monitor tracing shows fluctuations of the FHR baseline that are described as variability. Long-term variability is the waviness of the FHR tracing assessed over time and can be observed with external and internal fetal monitoring. Short-term variability (STV) is the “push-pull” effect of sympathetic and parasympathetic nervous system input and can be assessed only with a spiral electrode (Freeman & Garite, 1981; Martin, 1990; Murray, 1988; Olds et al., 1992; Tucker, 1992; West et al., 1993). Freeman and Garite (1981), Murray (1988), and Petrie (1991) state that variability is the most important characteristic of the FHR in predicting the status of a fetus. Normal variability should be observed after 28 weeks gestation (Petrie, 1991). The presence of normal variability is one of the best indicators of an intact pathway between the central nervous system and the heart (Murray, 1988; Petrie, 1991).
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I
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**,I#
...
..,
(1
I S
..t UI
Figure 3. ExternulJetul monitor tracingfor Case 2, u 311vear-oldwomun. gruvidu 11.paru I, at 36 weeks gestution. with premature rupture of memhrunes at 1250 a.m.
Finally, an assessment is made of accelerations and decelerations. A reassuring tracing indicates the presence of spontaneous accelerations and absence of late decelerations (West et al., 1993). Fetal bradycardia with the presence of such reassuring features as average variability and/or spontaneous accelerations indicates that a fetus is under a degree of stress but has enough oxygen and metabolic reserve to compensate (West et al., 1993). Fetal bradycardia accompanied by average variability is only a stressful incident and usually well tolerated by the fetus (Cabaniss, 1993; Gimovsky & Caritis, 1982; West et al., 1993). However, fetal bradycardia without such variability represents direct myocardial depression. This is a nonreassuring pat-
tern requiring immediate intervention (Gimovsky & Caritis, 1982; West et al., 1993). In our center, we observe for reassuring tracings using the external fetal monitor. When a nonreassuring tracing is noted, we consider using a spiral electrode and obtaining a scalp pH.
Interventionsfor Maternal Hypotbermk Three reports of persistent fetal bradycardia associated with maternal hypothermia in laboring clients are presented for review (see Cases 1, 2, and 3). The presence of L T V and STV remained constant in each episode reported. Initially, all three patients received the routine care provided to all laboring clients. They were assessed
~~
Figure 4 Externalfetal monitor tracingfor Case 2 at 8 55 a m Sterile vaginal examination showed 7 cm drlatation/ 80%effuced/O station
676 J O G N N
Volume 25, Number 8
Maternal Hypothermia and Fetal Bradycardia
in the labor and delivery triage area and then moved to an adjacent labor, delivery, and recovery room. Several different labor, delivery, and recovery rooms were used for these clients. The women were infused with room temperature intravenous solutions of lactated Ringer's or dextrose 5% lactated Ringer's solution. These three episodes were observed in heated and air-conditioned rooms. During discussions with other nursing staff members, it was mentioned that a retired nurse with many years o f labor and delivery experience had noted the correlation between fetal bradycardia and maternal hypothermia. Because this association was not common knowledge among our physicians or nursing staff, steps to correct maternal hypothermia were not implemented routinely.
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Figure 5 Muternal temperutureand,fitul heart ratejbr Cave 2.
Because of the potential for metabolic complications, a neonate experiencing cold stress may need to be assessed as frequently as every 15-30 minutes during the initial neonatal period.
As this correlation became more evident, the nursing staff and physicians intervened to increase the temperature of the mothers. Nursing measures included using warm fluids, warm blankets, stockinette caps, and socks. Intravenous fluids and blankets are stocked in warming cabinets in our unit. If further interventions were warranted, the nursing staff obtained a physician's order for a fluid warmer and/or a thermo-controlled blanket, which were used to produce successful results. In most cases, the mother's temperature began to rise. It was observed that the fetal bradycardia abated as the maternal temperature increased. The rectal temperature of the neonate also was within normal limits, except in Case 3, in which the maternal hypothermia was not resolved fully by delivery. In that case, the maternal temperature at delivery was 95.6"F ( 3 5 3 ° C ) degrees and the neonate's initial temperature was 96.0°F (35.6"C) degrees. The normal range for rectal temperature in a neonate is 97.8"F99.O"F (36.6"C-37.3"C) (Olds et al., 1992). This subnormal temperature can lead to neonatal cold stress.
Neonatal Risks Neonatal cold stress is an excessive heat loss that results in compensatory mechanisms being used to maintain core body temperature. The metabolic consequences of cold stress can be devastating and are potentially fatal to the infant (Olds et al., 1992). Because of the potential for complications, a neonate who experiences cold stress
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may need to remain in a thermo-controlled environment for several hours; rapid warming of the neonate can lead to apnea (Olds et al., 1992). Interventions during this initial neonatal period may include an evaluation for hypoglycemia and skin temperature assessments as frequently as every 15-30 minutes. This could interfere with newborn-family attachment. Parents can be present in the nursery while the neonate is under a radiant warmer, but such a situation is not ideal for the initial hours after delivery.
Nursing Implications Determination of the cause of persistent fetal bradycardia (as is done with fetal tachycardia) can help to establish the need for interventions. An investigation is recommended when persistent fetal bradycardia is noted (Cabaniss, 1993; Roberts, 1989). Assessment of the maternal temperature by either a tympanic or axillary mode may be more reliable than orally when oxygen is in use or ice chips or popsicles are being consumed. Perinatal standards of the American College of Obstetrics and Gynecologists call for assessing the mother's temperature every 4 hours during the intrapartum period (Freeman & Poland, 1992). When the membranes rupture, the mother's temperature should be assessed every 1-2 hours (Martin, 1990; Olds et al., 1992;West et al., 1993). If the cause of persistent fetal bradycardia is determined to be maternal hypothermia with n o attributable factors, nursing and medical interventions to increase the maternal temperature may be required before there is an alleviation of the fetal bradycardia. Maternal temperature assessments may be required hourly until resolution of the variance. A side effect of maternal hypothermia may be a slowing of the labor progress, as noted in Cases 1 and 3, when the transition phase lasted 3% hours and 4 hours, respectively. Observing for a correlation between fetal bradycardia and maternal hypothermia may assist the nurse in evaluating the fetus during the second stage of labor. If fetal bradycardia
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Figure 6. Exlernulfeul monitor Irucingjbr Cuse 3 a1630 a.m. S l e d e vaginal exminulion sbowed 4-cm dilutalion/ 100%eJaced/- 1 stufion.
persists into the second stage of labor, the presence of variable decelerations may concern the caregivers. When a deceleration occurs from an already significant low baseline, the fetus may not receive adequate perfusion of vital structures during the deceleration. In this instance, the caregiver would expect to find evidence of progressive development of hypoxic changes (Cabaniss, 1993).
Sum ma ry Using astute observation and the correlation between maternal hypothermia and fetal bradycardia, labor and delivery nurses can initiate appropriate interventions. Early interventions to correct the maternal hypothermic state before delivery can avoid possible neonatal problems. Preventing a state of newborn hypothermia, which can lead to problems for the neonate from cold stress, is a desired goal for perinatal nurses.
Case I A 22-year-oldgravida I, para 0, at 40 weeks gestation with spontaneous rupture of the membranes occurring at 1 a.m. was admitted to labor and delivery at 3:30 a.m. with
early labor (3-cm dilatation). Her vital signs at admission were blood pressure, 129/87; temperature, 95.8" F
Early interventions to correct the maternal hypothermic state before delivery can avoid possible neonatal problems.
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(35.5"C); pulse rate, 94; and respiration rate, 20. The FHR baseline was 105-115 bpm with a reassuring tracing on an external fetal monitor. The mother's physician and nurse were unable to ascertain a cause of the maternal hypothermia. Results were negative from blood tests ordered to rule out sepsis. Because it was winter, a social assessment was performed and the mother's home was noted to have heat. One milligram of butorphanol tartrate was given intravenously at 4:15 a.m. for labor pain, and epidural anesthesia was begun at 4 5 0 a.m. Her vital signs remained stable, with a temperature of 9 6 . 7 " (36.0"C) ~ and FHR of 90-1 10 bpm. A spiral electrode was placed on the scalp of the fetus at this time. Average LTV remained and STV was present (see Figure 1). At 6:15 a.m., the mother's cervical dilatation was 8 cm with 100% effacement. At 7:OO a.m., her temperature decreased to 95.6"F (35.3"C). Warm blankets, a stockinette cap, intravenous fluids via a fluid-warmer, and a thermo-controlblanket were used to conserve and increase the mother's body heat. A simultaneous increase in maternal temperature and FHR baseline was noted at 8:OO a.m. Slow cervical dilatation progressed. Pushing was initiated at 1O:OO a.m. when the cervix was dilated completely and the fetal head was at +1 station. The FHR baseline was now 115125 bpm, and the maternal temperature increased to 9 8 9 ° F (37.2"C). A viable boy was born 2 hours and 30 minutes later with Apgar scores of 6 and 8 at 1 and 5 minutes, respectively. The maternal temperature at delivery was 98.4' F (36.9"C), and the neonate's initial temperature was 99.1"F (37.3"C). This case shows how the correction of maternal hypothermia correlated with the correction of fetal bradycardia. The outcome of the neonate's core temperature was favorable.
Volume 25, Number 8
Maternal Hypothermta and Fetal Bradycardia
Figure 7. lnternul~talmonitor tracing and internal uterine pressure catheterjor Case 3 at 1050 a.m.
Case2 A 31-year-oldgravida 11,para I, at 36 weeks gestation with premature rupture of membranes, presented to the labor and delivery unit in early labor. At 12:46 a.m., her vital
signs at admission were blood pressure, 129/74; temperature, 98.7"F (37.0"C); pulse rate, 71; and respiration rate, 18. The FHR baseline was 130-140 bpm on an external fetal monitor, with a reassuring tracing (see Figure 3). An intravenous oxytocin infusion was begun. Ninety minutes later, the maternal temperature was 97.7"F (36.5"C) and the FHR baseline was 120-130 bpm. The maternal temperature continued to decrease during the next several hours, and the FHR baseline decreased simultaneously. A reassuring tracing continued to be present. Neither the nursing staff nor physician were able to
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Figure 8. Muternal temperature andfetal heart rate trucingfor Case 3.
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Case3
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A 26-year-old gravida 11, para I, at 39 weeks gestation was admitted to the labor and delivery unit in active labor (4-
1
cm dilatation). Her admitting vital signs were blood pressure, 130/72; temperature, 98.4"F (36.9"C); pulse rate, 83; and respiration rate, 20. The FHR baseline was 130140 bpm, with a reassuring fetal monitor tracing on an external fetal monitor (see Figure 6). Two hours later, the maternal temperature decreased to 96.4"F (35.8"C) and the FHR baseline was 110-125 bpm with minimal LTV. The transition phase began at 8:OO a.m. At 10:05 a m . , an intrauterine pressure catheter and a spiral electrode were placed by the physician. The maternal temperature continued to decrease, which concerned the
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diagnose a cause for this decrease in the maternal temperature. Intravenous butorphanol tartrate was given to the mother for pain at 3:30 a.m. At 7:OO a m . , an amnioinfusion for variable decelerations was begun via a fluid warmer per our unit protocol. A fetal scalp pH test performed at 8:50 a.m. was 7.31. At 9 0 0 a m . , the maternal temperature remained low at 95.6"F (35.3"C), with the FHR baseline at 100-110 bpm (see Figure 4). A thermocontrol blanket, another medical intervention, was applied at this time. A resulting increase in the maternal temperature to 97.8"F (36.6'C) was noted 1 hour later. The FHR baseline increased to 112-118 bpm. The thermo-control blanket was discontinued. During the next hour, the maternal temperature and FHR baseline returned to the admission range. Apgar scores for the neonate were 8 at 1 minute and 9 at 5 minutes. The neonate's initial temperature was 97.4"F (36.5"C).After correlating the decrease in the FHR baseline with maternal hypothermia, interventions were initiated, and again, a favorable outcome in terms of neonatal core temperature was obtained.
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physician and nursing staff. Three hours into the transition phase, the maternal temperature was 95.4' F (35.2"C),and the FHR was 95-110 bpm, with STVpresent (see Figure 7). Hydration with warm intravenous fluids began at 1O:OO a.m. for epidural anesthesia. N o relief was noted from the maternal hypothermia, and, therefore, the physician ordered a thermo-control blanket. At 10:30a m . , pushing began because cervical dilatation was complete and the fetal head was at +1 station. N o change in the maternal temperature or FHR was noted. Early decelerations with a decrease in the FHR down to 60 bpm were noted during the second stage of labor. A viable boy with Apgar scores of 6 and 8 was delivered after 30 minutes of pushing. The mother's initial temperature postpartum was 9523°F (35.5"C), and the neonate's initial temperature was 96.O"F (35.7"C). The neonate was placed under an infant warmer in the extended-care nursery. The neonate's temperature slowly increased to 98.O"F (36.7"C) 90 minutes after delivery. During this period, skin assessments every 15 minutes were required. Warm blankets were placed on the mother, and her temperature increased to 98.O"F (36.7"C) within 2 hours. This case shows the possible result when the correlation between maternal hypotherrnia and fetal bradycardia remains undiagnosed or when interventions are not initiated expediently. Although no complications developed, the potential for neonatal cold stress was present.
References
(Ed.), Anesthetic & obstetric management of high-risk pregnancy (pp. 210-259). St. Louis: Mosby-Year Book. Martin, E. J. (1990). Admission assessment of the laboring woman. In S. M. Glover (Ed.), Intrapartum Management Models: A Perinatal Education Program (pp. 59-98). Baltimore: Williams (G Wilkins. Murray, M. (1988). Antepartum a n d intrapartalfetal monitoring. Baltimore: Williams & Wilkins. Olds, S., London, M., Lk Ladewig, P. (1992). Maternal-Newborn Nursing (4th ed.). Redwood City: Addison-Wesley Nursing. Petrie, R. H. (1991). Intrapartum fetal evaluation. In S. G. Gabbe, J. R. Niebyl, & J. L. Simpson, (Eds.), Obstetrics: Normal &problem pregnancies (2nd ed., pp. 457-491). New York: Churchill Livingstone. Roberts, J. E. (1989). Managing fetal bradycardia during second stage of labor. MCN: American Journal of Maternal/Child Nursing, 14, 394-398. Rodis, J. F., Vintzileos, A. M., Campbell, W. A., Deaton, J. L., & Nochimson, D. J. (1987). Maternal hypothermia: An unusual complication of magnesium sulfate therapy. American Journal Obstetrics a n d Gynecology, 156(2), 435-436. Thompson, J., McFarland, G., Hirsch, J., & Tucker, S. (1993). Health perception-health management. In S. Schrefer (Ed.), Mosby's clinical nursing (pp. 1470-1473). St. Louis: Mosby-Year Book Tucker, S. (1992). Baseline fetal heart rate. In T. V. Schaik (Ed.), Pocket guide to fetal monitoring (2nd ed., pp. 65-82). St. Louis: C.V. Mosby Co. West, J., Chez, B. F., & Miller, F. C . (1993). Fetal heart rate. In R.A. Knuppel & J.E. Drukker, (Eds.), High riskpregnancy, a team approach (2nd ed., pp. 316-336). Philadelphia: W.B. Saunders.
Cabaniss, M. L. (1993). Fetal monitoring interpretation. Philadelphia: J.B. Lippincott. Freeman, R. K., (G Garite, T. J. (1981). Baseline shifts. In Fetal heart rate monitoring (pp. 63-68). Baltimore: Williams & Wilkins. Freeman, R. K., & Poland, R. L. (Eds.). (1992). Guidelines for perinatal care (3rd ed.) Elk Grove Village, IL: American Academy of Pediatrics. Gimovsky, M. L., & Caritis, S. N. (1982). Diagnosis and management of hypoxic FHR patterns. Clinics in Perinatology, H 2 ) , 313-324. Jadhon, M., 62 Main, E. (1988). Fetal bradycardia associated with maternal hypothermia. Obstetrics a n d Gynecology, 72(3), 496-497. Johnson, M., (G Saltzman, D. (1991). Cardiac disease. In S. Datta
Helene White Dodson is a staff nurse andpreceptor in Labor and Deltveryptgh-Risk Obstetric Care at Arnold Palmer Hospitalfor Chtldren G Women in Orlando, FL.
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Addressfor correspondence: Melanie J. Rets, RN, MN, CNS, Arnold Palmer Hospttal f o r Children G Women, Labor and Delivery MP 321,92 W.Miller St., Orlando, FL 32806. Melante J. Reis is a pertnatal clinical nurse specialist in Outcomes Management at Arnold Palmer Hospital f o r Chtldren G Women in Orlando, FL.