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An acceleration is a visually abrupt increase in the fetal heart rate (FHR) above the baseline with onset to peak of the acceleration less than 30 seconds .

For fetuses > 32 weeks gestational age the peak heart rate must be > 15 beats per minute (BPM) above the baseline and must last for > 15 seconds but less than 2 minutes from the initial change in heart rate to the time of return of the fetal heart rate to the baseline. For fetuses < 32 weeks of gestation the accelerations must have a peak heart rate > 10 beat and a duration of > 10 seconds but less than 2 minutes .

An acceleration >  2 minutes but less than 10 minutes in duration is called a prolonged acceleration.   An acceleration lasting > 10 minutes is a baseline change. Accelerations may be further categorized as episodic or periodic. Episodic accelerations occur independent of uterine contractions.  Periodic accelerations are associated with uterine contractions.  Accelerations may be present or absent in an otherwise normal category I fetal heart rate tracing.[1].

Accelerations are usually, but not always, associated with either spontaneous fetal activity, stimulation, or uterine activity [2-4]. Accelerations have also been attributed to partial umbilical cord occlusion caused by a baroreceptor-mediated response to decreased venous return [5].

The presence of either spontaneous or stimulated FHR accelerations reliably predicts the absence of fetal metabolic acidemia at the time they are observed provided the heart rate being recorded is truly the fetus and not the mother [1,6].  Periodic accelerations caused by partial umbilical cord compression are not as reassuring as episodic accelerations since continued cord compression may cause progression to a category II or category III tracing [10]. A rise in the fetal heart rate provoked by fetal scalp stimulation during a prolonged deceleration is of uncertain significance since the rise in heart rate is not by definition an acceleration.
The tracing below shows accelerations assocated with maternal pushing.

Although the accelerations in Figure 1  might be attributed to partial umbilical cord occlusion, fetuses typically show decelerations with pushing while mothers show accelerations in their heart rate when pushing. The heart rate could, therefore, be either fetal or maternal. In this situation (as well as in other situations where signal ambiguity might occur such as with a low baseline FHR or maternal tachycardia) placing a pulse oximeter on the mother,  and comparing the maternal heart rate (MHR) with FHR (Figure 2)  may help to clarify the source of the heart rate pattern being traced [7-9].

1. Macones GA, et al.  The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines. Obstet Gynecol. 2008 Sep;112(3):661-6.PMID: 18757666
2. Rabinowitz R, The relation between fetal heart rate accelerations and fetal movements.
Obstet Gynecol. 1983 Jan;61(1):16-8.PMID: 6823344
3. Vintzileos AM, et al., Relation between fetal heart rate accelerations, fetal movements, and fetal breathing movements.
Am J Perinatol. 1986 Jan;3(1):38-40.PMID: 3510628
4. Sadovsky E, et al. ,The relationship between fetal heart rate accelerations, fetal movements, and uterine contractions.Am J Obstet Gynecol. 1984 May 15;149(2):187-9.PMID: 6720797
5. Lee CY, Di Loreto PC, O'Lane JM.A study of fetal heart rate acceleration patterns.
Obstet Gynecol. 1975 Feb;45(2):142-6.PMID: 1118084
6. Skupski DW, et al. Intrapartum fetal stimulation tests: a meta-analysis.Obstet Gynecol. 2002 Jan;99(1):129-34. PMID: 11777523
7. Sherman DJ, Characteristics of maternal heart rate patterns during labor and delivery.
Obstet Gynecol. 2002 Apr;99(4):542-7.PMID: 12039107
8. VAN Veen TR, et al,. Maternal heart rate patterns in the first and second stages of labor.
Acta Obstet Gynecol Scand. 2012 May;91(5):598-604.PMID: 22313165
9. Neilson DR Jr, et al., Signal ambiguity resulting in unexpected outcome with external fetal heart rate monitoring.Am J Obstet Gynecol. 2008 Jun;198(6):717-24. .PMID:
10. Gaziano EP, et al. FHR variability and other heart rate observations during second stage labor.
Obstet Gynecol. 1980 Jul;56(1):42-7.PMID:

Friday, November 11, 2011

Five-Level Classification of Intrapartum Fetal Heart Rate Patterns

The National Institute of Child Health and Human Development has defined three categories of intrapartum fetal heart rate patterns
  • Category I     Normal
  • Category II    Indeterminate
  • Category III   Abnormal

Jackson M and coworkers reviewed the fetal heart rate data and newborn outcomes of women in term labor. They found the category I fetal heart rate pattern to be the most common during labor occurring 77.9% of the time. The category II pattern occurred 22% of the time during labor,  and the category III pattern occured rarely, only 0.004% of the time during labor.

There has been some concern that the non specific nature and large number of fetal heart rate patterns within category II diminishes its usefulness as an indicator of fetal condition. Considering the high likelihood of category II fetal heart rate patterns during labor a better system for evaluating the significance of these patterns might help in reducing the number of cesarean sections performed for nonreassuring fetal status. The classification developed by Parer and Ikeda may be a step in the right direction.
The classification system developed by Parer and Ikeda is  a color coded, five-category scheme based on published outcome risks related to specific fetal heart rate characteristics. The Parer and Ikeda  system essentially divides the indeterminate category into three additional risk levels and considers  the depth and length of the decelerations in evaluating the risk for the development acidemia.

The chart below  is a condensation of the Parer and Ikeda Five-Level Classification of intrapartum fetal heart rate patterns including recommended actions.

Macones GA et al., The 2008 National Institute of Child Health and Human Development Workshop Report on Electronic Fetal MonitoringUpdate on Definitions, Interpretation, and Research Guidelines Obstetrics & Gynecology 2008;112:661-666 PMID:18757666

Jackson M, et al. Frequency of fetal heart rate categories and short-term neonatal outcome. Obstet Gynecol. 2011 Oct;118(4):803-8.PMID:21897312

Parer JT, Ikeda T.A framework for standardized management of intrapartum fetal heart rate patterns. Am J Obstet Gynecol. 2007 Jul;197(1):26.e1-6.PMID:17618744

Parer JT, Hamilton EF.Comparison of 5 experts and computer analysis in rule-based fetal heart rate interpretation.Am J Obstet Gynecol. 2010 Nov;203(5):451.e1-7. Epub 2010 Jul 15.PMID: 20633869

Barber EL, et al. Indications contributing to the increasing cesarean delivery rate.
Obstet Gynecol. 2011 Jul;118(1):29-38. PMID:21646928

Sunday, August 29, 2010

A Patient With Possible Severe Preeclampsia

A 34 year old Gravida 3, Para 2 with a history of 2 cesarean deliveries and chronic hypertension was seen in the office at 25 weeks' for a routine examination. She was noted to have a blood pressure of 210/105 mm Hg with 4 + proteinuria on urine dipstick. She did not have proteinuria on urine dipstick in the past and a 24 hour urine collection at 14 weeks' showed 300 mg of protein. Her fetus measured 22 weeks' and had oligohydramnios. Doppler examination of the umbilical artery showed absent end diastolic flow. She denied headache, epigastric pain, visual complaints, cough, and shortness of breath. She had been taking methyldopa 500 mg orally twice daily for the control of her blood pressure.

She was admitted for treatment of her severe hypertension and evaluation for possible superimposed preeclampsia. She was given a 4 gram loading dose of magnesium sulfate followed by 2 grams per hour infusion. She was also given Celestone 12 mg IM. Over the course of one hour she received three doses of hydralazine 5 mg IV followed by labetalol 20 mg , 40 mg, and 80 mg. Her blood pressure was decreased to 156 / 90 mm Hg.

(20 mg IV is the maximum cumulative dose of hydralazine recommended for the treatment of acute severe hypertension in pregnancy. 220 mg IV is the maximum cumulative dose of labetalol recommended for the treatment of acute severe hypertension in pregnancy [1]).

Platelet count: 120 X 10 9/L
Alanine aminotransferase , ALT, SGPT  : 33 U/L (0.55 ┬Ákat/L)
Aspartate aminotransferase ,AST, SGOT  : 32 U/L (0.53 ┬Ákat/L)
Urinalysis significant for 3+ protein, trace blood.
Urine toxicology screen: Negative

Two hours after admission she began to complain of abdominal pain and cramping. Her blood pressure was 180 /100.

Her fetal heart tracing showed the following pattern:

What would you do next?

1. Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol 2000;183:S

Sunday, April 11, 2010

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Friday, February 12, 2010

Late Decelerations

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A deceleration is a decrease in the fetal heart rate below the fetal baseline heart rate. An early deceleration is defined as a waveform with a gradual decrease and return to baseline with time from onset of the deceleration to the lowest point of the deceleration >30 seconds. The nadir of the early deceleration occurs with the peak of a contraction.
A late deceleration also has a waveform with a gradual decrease and return to baseline with time from onset of the deceleration to nadir >30 seconds. However, the late deceleration is "shifted to the right" of the contraction.

The onset of the deceleration occurs after the beginning of the contraction, and the lowest point of the deceleration occurs after the peak of the contraction.
The difference in the timing of early decelerations and late decelerations relative to the contraction may be explained by the underlying mechanism for each of these decelerations.
Early decelerations appear to be caused by vagal discharge produced when the head is compressed by uterine contractions. The onset and depth of early decelerations mirror the shape of the contraction, and tend to be proportional to the strength of the contraction.
Late decelerations occur when a fall in the level of oxygen in the fetal blood triggers chemoreceptors in the fetus to cause reflex constriction of blood vessels in nonvital peripheral areas in order to divert more blood flow to vital organs such as the adrenal glands, heart, and brain. Constriction of peripheral blood vessels causes hypertension that stimulates a baroreceptor mediated vagal response which slows the heart rate. The time consumed in this two step process accounts for the delay in the timing of the deceleration relative to the contraction.
Late decelerations with good variability ("reflex lates") are sometimes caused by excessive uterine contractions or maternal hypotension which may be alleviated by correcting the underlying cause. In conditions with reduced placental exchange such as intrauterine growth restriction (IUGR) measures to improve blood flow and oxygen delivery to the fetus may not be as effective.
If oxygen continues to be limited (hypoxia) to the fetal tissues acidosis can develop as result of increased anaerobic metabolism. Significant levels of acid in the blood (acidemia) can suppress the fetal nervous system leading to decreased variability and direct myocardial depression made evident by shallow late decelerations. If myocardial depression is severe enough, late decelerations may be absent all together

Etiologies of Late Decelerations

Excessive uterine contractions
Maternal hypotension
Maternal hypoxemia (asthma, pneumonia)
Reduced placental exchange as in:
    Hypertensive disorders Diabetes IUGR Abruption

1. Cabaniss ML ,Ross MG.Fetal Monitoring Interpretation 2nd ed.Philadelphia, Lippincott Williams & Wilkins, 2009
2. Harris JL, Krueger TR, Parer JT Mechanisms of late decelerations of the fetal heart rate during hypoxia. Am J Obstet Gynecol. 1982 Nov 1;144(5):491-6. PMID:7137235
3. Murata Y, et al.  Fetal heart rate accelerations and late decelerations during the course of intrauterine death in chronically catheterized rhesus monkeys. Am J Obstet Gynecol. 1982 Sep 15;144(2):218-23.PMID:7114133
4. Gaziano EP, Freeman DW Analysis of heart rate patterns preceding fetal death. Obstet Gynecol. 1977 Nov;50(5):578-82. PMID:909663

Tuesday, January 26, 2010

Review of Three-Tier Fetal Heart Rate Interpretation System

Category I : Normal.
The fetal heart rate tracing shows ALL of the following:

Baseline FHR 110-160 BPM, moderate FHR variability, accelerations may be present or absent, no late or variable decelerations, may have early decelerations.

Strongly predictive of normal acid-base status at the time of observation. Routine care.

Category II : Indeterminate.

The fetal heart rate tracing shows ANY of the following:

Tachycardia, bradycardia without absent variability, minimal variability, absent variability without recurrent decelerations, marked variability, absence of accelerations after stimulation, recurrent variable decelerations with minimal or moderate variability, prolonged deceleration > 2minute but less than 10 minutes, recurrent late decelerations with moderate variability, variable decelerations with other characteristics such as slow return to baseline, and "overshoot".

Not predictive of abnormal fetal acid-base status, but requires continued surveillance and reevaluation.

Category III: Abnormal.

The fetal heart rate tracing shows EITHER of the following:

Sinusoidal pattern OR absent variability with recurrent late decelerations, recurrent variable decelerations, or bradycardia.

Predictive of abnormal fetal-acid base status at the time of observation. Depending on the clinical situation, efforts to expeditiously resolve the underlying cause of the abnormal fetal heart rate pattern should be made.

Case 1
G1P0 . Induction for preeclampsia at 37 weeks.

Case 2
G2P1. Arrived in active labor at 40 weeks

Case 3
G1, P0, 34 weeks gestation admitted to Labor and Delivery with SROM with moderate amount of pink tinged fluid.

Macones GA et al., The 2008 National Institute of Child Health and Human Development Workshop Report on Electronic Fetal MonitoringUpdate on Definitions, Interpretation, and Research Guidelines Obstetrics & Gynecology 2008;112:661-666 PMID:18757666