Labor and Delivery Resource Library

Additional Information Resources for L&D Clinicians

Use these resources to learn how organizations use best practices and benchmarking to improve performance.

The following resources are helpful for those looking to incorporate unit and care management strategies others are using to improve key obstetric benchmarks.

Early Warning Systems

The Institute for Healthcare Improvement calls them “scorecards that save lives.”  Originally created in answer to research finding that 40-50% of maternal deaths are potentially preventable, early warning systems seek to standardize clinical assessment and to facilitate recognition of maternity patients who have or are developing critical illness.  Non-obstetric early warning systems have been use in Europe, especially Great Britain, for over twenty years.  Systems adapted to obstetrics have started to gain traction in the US relatively recently.

There are two types of early warning systems.  Single parameter systems rely on carefully defined threholds.  Multiple parameters systems, often using weighted algorithms, result in a composite score that triggers protocol activities.  Because most systems are manual, the type used is often a balance between practicality and clinical impact.

(See how PeriWatch Vigilance™ provides easy-to-use, easy-to-implement way to leverage the impact of early warning systems.)

Following are links to published information on the design and use of obstetric early warning systems:

Other Reading:

The Category II Management App, a free web-based app (not-downloadable) offered exclusively by PeriGen, is based on published research and designed for US usage to help support the management of patients with FHR tracings in category II (present in over 80% of labors).

Only 4-8 clicks get you the suggested outcome and the app takes seconds to use.

  • Answer a few questions about the tracing and labor status
  • The application processes the data through the algorithm and presents its conclusion along with the publication’s original image.

This online app (not for download) can be used as often as needed on any computer or mobile device.

Register for the Category II Management App
(Before launching the web tool please read this important information.)

Any questions or feedback, email

A Message from Thomas Garite, MD
Chief Medical Officer:

“Category II fetal heart rate tracings are common and cover a wide spectrum ranging from relatively minor findings to more significant combinations that require very different clinical management. This app based on a researched algorthm represents a practical set of management guidelines for clinicians to consider as they care for women in labor. The algorithm was designed in accordance with a fundamental premise in patient safety circles – that standardization and simplification of critical care processes promote better outcomes. Please do read the full publication that describes a number of important concepts that clinicians must also include in their clinical reasoning. No simple algorithm can handle every unusual circumstances or rapid change in the tracing. We look forward to your feedback and hope it will be a useful tool for clinicians to access on their smart phones when managing patients whose tracings are in Category II.”

“We present an algorithm for the management of category II FHR patterns that reflects a synthesis of available evidence and current scientific thought. Use of this algorithm represents one way for the clinician to comply with the standard of care, and may enhance our overall ability to define the benefits of intrapartum FHR monitoring.”

Reference Publication:
Intrapartum management of category II fetal heart rate tracings: towards standardization of care. Clark SL, Nageotte MP, Garite TJ, Freeman RK, Miller DA, Simpson KR, Belfort MA, Dildy GA, Parer JT, Berkowitz RL, D’Alton M, Rouse DJ, Gilstrap LC, Vintzileos AM, van Dorsten JP, Boehm FH, Miller LA, Hankins GD. Am J Obstet Gynecol. 2013 Aug;209(2):89-97. doi: 10.1016/j.ajog.2013.04.030. Epub 2013 Apr 27

This collection of resources provides guidance to L&D unit leads on providing consistent standards of care:

When asked about their greatest challenges with existing EFM systems, labor & delivery clinicians consistently cite integration with their EHR.  In keeping with Stephen Covey’s (Seven Habits of Highly Effective People) rule of “seek first to understand,” following are resources for understanding the mechanics and practices for integrating electronic fetal monitoring systems with major EHRs.

Click to view video transcript

The Joint Commission on Accreditation of Healthcare Organizations (JCAHO) indicate that inadequate communications between providers or between providers and patients/families is the root cause of 60% to 70% of investigated sentinel events in medicine.  When 47 perinatal deaths were investigated by JCAHO, poor communication was identified as the root cause in 72% of these adverse events.

One of the most common challenges experienced by labor & deliver management is maintaining efficient communications between team members, while consolidating a wide range of skill sets and personalities into a cohesive, effective unit.  Here are a few information resources that may help you meet this challenge.  Please feel free to suggest more.

Team-Building Tools & Tips

The following information resources provide educational information on assessing labor progress, as well as the latest research on labor curves:

The following is a compilation of information resources providing practical, actionable strategies for fine-tuning your patient safety initiatives:

The Institute of Medicine defines protocols, or clinical guidelines, as “systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical situations.”  The following information resources aim to help labor & delivery unit directors, chair people, and risk managers understand, leverage, and improve protocol compliance.

Shoulder Dystocia

Shoulder dystocia is typically defined as a vaginal birth where the baby’s shoulders get “stuck,” requiring extraordinary maneuvers to delivery the fetus. The incidence of shoulder dystocia varies based on fetal weight, maternal weight, and the presence of diabetes. Complications associated with shoulder dystocia include postpartum hemorrhage, maternal lacerations, and brachial plexus palsies.

The electronic fetal monitoring (EFM) resources below have been compiled from a review of materials readily available on the Internet.  Although PeriGen is not responsible for the creation of this content — or for its continued availability and quality — they provide a comprehensive curriculum for clinicians seeking to gain a basic understanding of EFM.  In addition to these EFM training resources, we’ve found several general, free online training resources of use:

Electronic fetal monitoring definition: 

Electronic fetal monitoring or EFM is the practice of measuring and displaying fetal heart rate and contraction rate during labor.  Traditionally, the output of EFM takes the form of tracings — a visual display of the fetal heart rate on top and the contraction rate on the bottom.

PeriGen's Cues offers cutting-edge L&D strip analysis

Screenshot of an EFM tracing with feature analysis generated by the PeriWatch system

Like much technology, electronic fetal monitoring has progressed rapidly.  The latest EFM software offers  specialized displays so a detailed view of the tracing can be seen simultaneously with a longer term overview for trend analysis, pattern recognition, and color-coded notifications when specific combinations of EFM patterns are present. All of these advances help labor & delivery clinicians to spend less time on manual calculations, support improved care decisions, and better manage multiple patients.

This technology adds statistical analysis to the traditional EFM display to highlight abnormal patterns, yield meaningful summary information, and display the meaningful interaction between contractions and fetal heart rate via color-coded visual cues.

Figure 2. PeriCALM Patterns display showing the analysis related to uterine tachysystole.

Figure 2. PeriWatch Cues display showing the analysis related to uterine tachysystole.

Some of the most recent technology adds an even greater depth of statistical interpretation to labor progress, comparing a single patient’s measurements to a large population of others sharing similar characteristics.

EFM Education: PeriCALM Curve Labor Progress Analsysis Software

PeriCALM Curve offers labor progress analysis

*PeriGen is approved by the California Board of Registered Nursing, Provider Number CEP16729. Video completion via a single computer/device per user is required for credit achievement.  Once video completed, a web link is provided for completion of a mandatory course evaluation.  Once evaluation is finished, an online certificate of completion is provided for printing and retention.

Workflow is defined as a set of tasks and resources need to accomplish to meet a goal.  Defining and conforming to a set of processes enables a team to consistently achieve organizational objectives.  Typical workflows in a labor & delivery unit include admission, documentation, and filling laboratory orders.  Following are information resources on defining and optimizing workflows for labor & delivery teams.

Following are items of broad interest to labor & delivery clinicians:

The PeriGen L&D Continuing Education Program

Course: Understanding Uterine Activity
Presenters: Michelle Flowers, RNC-OB and Emily Hamilton, MD CM
Time: One Hour
Contact Hour: 1.0*
Slides: Click Here
Objectives: Review nomenclature and definitions associated with uterine activity, discuss basic etiology principles related to uterine tachysystole, and analyze uterine tachysystole’s impact on fetal heart rate.

Welcome to this continuing education session.  Our presenters today are Michelle Flowers and Rr. Emily Hamilton.
Michelle Flowers serves as PeriGen program manager and clinical consultant.  She’s got 20 years on experience in OB that includes coordination of clinical
quality programs.  She’s been an educator for obstetric services and L&D charge nurse.  More recently she’s focused on designing and executing OB documentation workflows and training programs.  Her education credentials include intermediate and advanced fetal monitor instruction and work as a ICEA-approved trainer.  She’s a certified childbirth educator and an AAPRP instructor.
Dr. Hamilton is PeriGen’s senior vice president of clinical research.  She’s an experienced obstetrician, as well as an adjunct professor of obstetrics and gynecology at McGill.  She is the inventor of PeriGen’s decision support system, holding 32 US and international patents for her research work.  She speaks
widely on the use of technology to improve obstetric outcomes regularly around the world and is also extensively published in the major peer-reviewed journals.
First, Michelle will take you the objectives of today session.  It does award one continuing education unit and we’ll discuss next steps at the end.
Thank you everybody for your time today as we discuss and further our understanding of uterine tachysystole and uterine activity.  So first we would like to the
review our objectives for today’s session:
  • Review the definitions related to uterine activity
  • Review the etiology and physiology of uterine tachysystole
  • Analyze the impact of uterine tachysystole on the fetal heart rate
So, what are uterine contractions?  Uterine contractions are quantified as the number of contractions present in a 10-minute window averaged over 30
minutes.  To help prepare for today’s session, we would like to discuss and review some basic terminology and physiology associated with uterine contractions so let’s begin with frequency.
Frequency:  How often contractions occur counted from the beginning of the contraction to the start of the next contraction and measured in minutes.
Duration:  How long contractions last. Duration is assessed from the beginning of the contraction to the end of contraction and measured in seconds.
Intensity: How strong the contractions are.  The strength of the contraction.  It’s determined by palpation if we’re monitoring externally and typically noted as mild, moderate or strong.  When using external monitors palpation, the abdomen must be palpated and the patient queried regarding strength of contractions. However if we’re using an IU PC, we measure that with millimeters of mercury.  Here in North America that’s the most common unit of measurement when employing an internal.
Resting tone:  The measurement of the uterus at rest and or in between contractions.  It’s assessed, again, via palpation or via millimeters of mercury if using internal monitors.
When speaking about uterine palpation, it’s good to know that the palpation of the uterus before, during and after a contraction and enlisting input for the laboring woman provides us with information critical to understanding a complete assessment of the quality and strength of contractions.  So one way we can go about assessing palpation is by using something all of us have at our fingertips – our faces.   So whether we’re training a new nurse or helping our patient and their spouses and significant others to identify the difference between a mild, moderate or strong contraction, we can utilize our faces as a guide when assessing.  For instance, for a mild contractions such as we see at the beginning of the labor process, we can use the tip of our nose.  The tip of your nose is easily indented.  A moderate contraction palpates more like your chin.  So it’s slightly indented but yet firmer than you would find the tip of the nose. We compare palpation for a strong contraction to your forehead,  Your forehead cannot be indented With palpation that would be indicative of a strong contraction. So when palpating the
abdomen during the contraction, if it is firm and cannot be indented, it that would be considered a strong contraction.  We see this during the active phase and towards the end of the labor process.
The art of palpation is a very useful tool and helps us determine strengths of contractions as well as asking our laboring women to help us with the pain scale throughout the labor to determine if our contractions are increasing in intensity.
Moving on, let’s talk a little bit more about contractions to provide a framework for the rest of today’s discussion.  Contractions generate inner uterine pressure.  They cause the retraction, effacement and dilatation of the cervix.  They help facilitate the descent and the birth of the fetus and affect the maternal blood flow through the uterine myometrium, decreasing it and causing the transient intermittent interruption in oxygenation to the fetus.
A normal contraction pattern is five contractions or less in ten minutes.  We’ll be talking about the difference between a normal contraction pattern versus a tachysystolic contraction pattern.
Let’s dive a little deeper into resting tone.  Resting tone is measured, again, by millimeters of mercury when using an IUPC or by palpation if assessing externally.  A normal resting tone helps to assist us in maintaining adequate fetal oxygenation by giving the fetus a period of relaxation between contractions and and allowing reoxygenation to occur.   Hypertonus is an elevated resting tone exhibited by a uterus that palpates firm and is are more hardened and doesn’t return to its precontraction soft state.  If using an internal monitor such as IUPC, this would be pressures to or greater than twenty to twenty-five millimeters of mercury.  If we were, for instance, inducing a woman and we did not see the resting tones coming back to precontraction state, we would need to adjust and give her that period of rest.
So, when we’re counting and gauging for our internal monitors so we have two units of measurement. We measure in ten minute segments and one way would be to measure the peak intensity or amplitude of each contraction in millimeters of mercury and add that together. Another, for yur MVUs, is to measure the peak intensity or amplitude in millimeters of mercury for each contraction in a 10-minute period, add those numbers together and subtract the difference between the amplitude and the resting tone at the peak of the contraction to give us the MVU.  For example, if you had three contractions each with an amplitude of 80, 80 and 75 respectfully with a 10 millimeter of mercury baseline in essence we would say 80 from 10 would be 70 for the first contraction and 80 from ten would be 70 for the second.  Then 75 from 10 would be 65.  If we take the sum of the three together that would be seventy plus seventy plus 65, giving us 205 MVUs.   MVU’s are the most common method of measurement here in North America, but we wanted to show that there are a few others methods out there in the marketplace.
We as a whole use MVUs when we’re counting out or in documenting the units of measuremen.  Again, the example provided that we take the amplitude, subtract the baseline, and add the numbers together within that ten minute segment to give us a estimation of what we’ve seen within that 10 minute period.
Let’s talk a little bit about the physiology of contractions during labor.  The uterus is divided into two functional segments.  The upper and the lower segment.  The upper segment is considered the active portion of the uterus during the labor process and it contains the pacemaker regions where contractions originate.  Currently there’s been no specific pacemaker site that we can point to that contractions come from but we do know they originate in these pacemaker regions and that successive contractions tend to cause the smooth muscle fibers in that upper region to shorten and thicken with successive contractions.  Likewise, they pull and retract on the lower more passive uterine segment causing it to thin and shorten, pulling on the cervix stem to help it to dilate and efface. We also know that, at the beginning of  labor, various hormonal changes occur such as an increase in the corticotropin-releasing hormone, a decrease in progesterone, and an increase in estrogen prostaglandin and oxytocin.  Together this process causes the uterine myometrium to go from a quiet to a more active state.  Contractions
therefore result when there is a coordinated propagation of myometrium contractions starting in the fundus of the uterus.
That being stated, let’s take a glance at the intramyometrium pressures effect on the blood flow.  You know that during the contraction the maternal blood flow is reduced.  This is directly related to the intra uterine myometrial pressure.  Once that pressure exceeds 35 to 60 millimeters of mercury those spiral arteries begin to be compressed.  This entire process begins to have an effect on the fetal compensatory mechanisms.  Remember, however, a healthy fetus has twice the reserve required to navigate the birth process.  A couple of things come into play here.  Extrinsic factors that impact the fetal heart rate and intrinsic factors that can affect a fetal heart rate pattern. Extrinsic to the fetus means factors outside of the fetus and intrinsic means factors internal to the fetus.
Let’s take a look at those.  Some maternal entrance extrinsic factors include maternal oxygenation status in the adequacy of maternal hemoglobin levels and cardiac output.  Factors that would decrease the maternal cardiac output or o2 content will have an impact on the the fetal extrinsic factors and help  determine blood flow to the uterus.  Some things to consider here:  Maternal hyper or hypotension, asthma, CHF, cardiac defects, hypobolemia from conditions that result from things like abruption, so any of those things can have an impact on the extrinsic maternal influences.  Now let’s take a look at uteral-placental perfusion.  You know uteral-placental perfusion is impacted by the structure and function of the placenta and its surface vessels so things like increased uterine contractions or  hypertonus come into play here.  The conditions that would impact this would be drug-induced oxytocin hypertonus or tachysystole.  An abruption causing the tachysystole could have a play.  Maternal condition such as hypertension, postdates, placental infarc such as we see with smoking.  Diabetes or any basal constriction type factors can have an impact on your uteral placental perfusion.
Thirdly, let’s look at umbilical circulation.  To discuss umbilical circulation, let’s do a brief review of the umbilical circulation.  The umbilical cord would normally contain three vessels — two arteries and one vein. The vein carries oxygenated blood from the placenta to the fetus.  Arteries carry de-oxygenated blood from the fetus to the placenta.  Any abnormalities of the cord or cord compression can affect the circulatory process.  What are some factors that we would be speaking of?  Things like the contractions, tachysystole, cord knots, nuca cords could affect the cord or the circulatory process can have a play with umbilical circulation and getting the oxygen back to the fetus.  Next would be ambiotic fluid.  That’s the amount of fluid within the uterus,  We all know the ambiotic fluid provides a cushion to the cord into the fetus during the birth process.  So be thinking of anything that might have a play there.
Let’s take a look at some intrinsic factors impacting fetal heart rate patterns.  Typically when we’re talking intrinsic factors we’re speaking of the fetal circulatory system and the fetal heart rate control in the fetal adaptive compensatory mechanisms.  Let’s do a brief review here as well.  So as we know oxygenated blood from the placenta flows through shunts in the fetal systemic circulatory system.  This allows for the preferential blood flow streaming patterns that we see that
prevent mixing of oxygenated and de-oxygenated blood.  When we’re speaking of fetal circulation, we know that fetal blood has an increased hemoglobin concentration that allows greater O2 carrying capacity.  You know that fetal hemoglobin has a high affinity for O2 and that the fetus has a greater cardiac output at a higher heart rate than the adult which allows rapid circulation. This entire process facilitates O2 transport to fetal tissues.  Decreased fetal heart rate
has an impact on the myocardium allowing it to decrease O2 consumption.  This redistribution of fetal blood flow permits preferential shunting to vital organs when the fetus is compromised.  Preferential shunting as well as decreased O2 consumption helps the fetus tolerate the stresses of labor and the birth process.
With fetal heart rate control, we know that it’s controlled by the parasympathetic and sympathetic nervous system.  The parasympathetic is largely in control at
term of pregnancy and the primary controller of variability.  Recognizing moderate variability indicates a well oxygenated fetus without acidosis.  Adaptation supports effective exchange of respiratory gases and aerobic metabolism.  The fetus has a compensatory reserve.  We know that the placental transfer capacity at 100% indicates the fetus has two times the reserve needed to navigate the birth process.  Once that capacity falls to 75%, we start to see HGA or “small-for-gestational-age” or IUGR. At 50% so when we would start to see fetal compromise.
Let’s look then at uterine tachysystole. Uterine tachysystole is defined as greater than five contractions in ten minutes averaged over 30 minutes.  A mathematical equivalent to that would be greater than 15 contractions in 30 minutes.  So what are some causes of tachysystole?  We know that one of the most well known would be an iatrogenic effect of induction and augmentation.  If you see a pattern and you feel that it is indeed tachysystole and the woman is being induced, one of the prime interventions would be to stop the induction agent.  If we cannot stop it then this patient might be a candidate for our beta sympathomimetic drugs in order to space those contractions out.  It can also be a result of spontaneous causes such as inner uterine infection and that there’s an irritation of the myometrium by the bacterial toxin.  Tachysystole has also been noted with the use of cocaine.  Tachysystole can also come from an unknown etiology.  We don’t know the cause.  The primary goal here is to recognize the pattern and be able to implement our inner uterine resuscitation measures to stop the pattern, so to be able to intervene and space the contractions out, allowing our fetus to recover and employee compensatory mechanisms or intervene
prior to those being necessary.
I would now like to hand the presentation over to Dr. Emily Hamilton so she can give us a deeper dive into the physiology behind uterine tachysystole.  We hope you will find the brief review of basic functioning definitions helpful as we proceed to go deeper into the physiology of uterine activity.
Dr. Hamilton: Thank you Michelle.
This is a graph taken from women in labor and you see the fetal heart rate on top, contractions on the bottom and the red line is demonstrating the babies
transcutaneous oxygen saturation.  The vertical arrows that are falling are there to show how oxygen levels at the fetal level change in timing in respect to the contractions.  You can see that the lowest level is a little bit after the contraction.  That is, during the contraction as Michelle mentioned, uterine blood flow is reduced through the myometrium.  Less oxygen delivery to the baby, and once the contraction has passed that interval of space blood is transmitted to the baby and we see a slight dip in the fetal oxygen saturation but normal babies will tolerate that very well.
Here is another experiment.  This is an experiment using fetal sheep.  It’s actually an experiment in which the fetal sheep have complete cord compression.  Now that’s not the same as the contraction of course but it does demonstrate a very severe form of impaired oxygen delivery to the baby.  This experiment is very illustrative of what happens when that happens very frequently.  In the first experiment, the compressions were one minute in duration and they occurred every five minutes.  Very severe.  Complete.  You can see the fetal sheep develop severe decelerations but all of these sheep despite four hours of this happening  maintain normal pH and were healthy at birth.  In the second panel, exactly the same experiment except the occlusions now happened two and a half minutes apart.  You can see again very severe decelerations as outlined in red.  Every single one of these fetal sheep developed severe acidosis.  In fact, every single one of these sheep develop brain lesions.
So if the compressions are severe and frequent, the fetal sheep does not have time, even with good compensatory mechanisms, to completely compensate for the reduction in oxygen delivery.  So when we are considering the effect of contractions it is important to consider that oxygen available to the baby correlates with contraction strength.  Higher contraction pressures mean less blood, with the duration of the contraction, longer contractions, and that impediment lasts longer and the interval because that’s when the baby can recover.  So reperfusion time is very important to restore oxygen levels in the interval of space before the next contraction begins.
What is the incidence of uterine tachysystole?  Well, you can see here 6 different studies and 6 different instances.  I’d like to begin with the paper by Bakker because it’s one which is very frequently quoted in any discussion of uterine tachysystole.  In this study, there were two groups of patients:  A control group when pH was normal and an adverse outcome group where the babies had acidosis pH of less than 7.11.  Using computer analysis they counted and calculated the frequency of contractions and you can see that the average frequency was 4.8 in the control group and 5.0 per 10 minutes in the acidotic group  and that
was different.  Babies with acidosis tend to have more contractions than those who were normal in the first stage and there was also a difference in the second stage.   5.2 in 10 minutes in the control and 5.5 in those with acidosis.  Again, acidosis was associated with more contractions than babies who were normal.  Now in this particular study, the actual incidence wasn’t reported but it must have been a very high incidence of uterine tachysystole because if on average your number of contractions per 10 minutes is more than five for ten minutes that means half of your patients are having even more and half of your a few patients are having less so one would estimate that the incidence of tachysystole in this study was somewhere around 50%.
Now let’s look at some of the other studies and you can see quite a variety here.  Dr. Rice Simpson looked at the incidence in patients undergoing induction of labor and found it to be around a quarter of the patients.  These other studies are involving patients not necessarily induced, but a mixture of induced and
spontaneous.  You can see rates that range anywhere from 13% up to 98%. The Kunz study is very much an outlier.  I don’t think any of us have experienced that in almost all patients with inductions that term will develop uterine tachysystole.  Nevertheless, it is one of the publications, one of the smallest studies, on this topic.   So, uterine tachysystole is, in fact, fairly frequent.
Now in the paper bySmith et al they also look at how long did the uterine tachysystole last and on the horizontal axis here you can see different durations of uterine tachysystole.  So, about 5 percent of mothers ha uterine tachysystole which just lasted 30 minutes.  That is, it merely appeared and within the next 10 minutes was gone.  A smaller percent lasted 40 minutes, 50 minutes, 60 minutes.  About only 4 percent of patients will have uterine tachysystole that will go on
beyond an hour.  Far different from those animal experiments that I showed you earlier.  So while it’s relatively frequent, it’s generally fairly transient.
All right.  Let’s look at the outcome of the babies depending upon the presence or duration of uterine tachysystole. In the group that had no uterine tachysystole,  in a large study, 5,000  or 1.3 percent developed neonatal depression.   What do we mean by that?  Babies where the base deficit was over 10 or the five-minute APGAR was 6 or less.  In the group who had any tachysystole about one percent developed neonatal depression.  When the uterine tachysystole was less than an hour, .7% and over an hour 1.9%.  So you can see a tendency that the rate of depression is greater when it lasts longer, but even over 60 minutes it’s relatively uncommon.
In this study we looked also at rates of uterine tachysystole depending upon the utilization of oxytocin and the highest rate, in fact a number of very similar to what Dr. Rice-Simpson found, just under a quarter of the patients with augmentation had uterine tachysystole.  Now, let’s look at how many had neonatal depression in those three groups and you can see that it’s less than 2% and relatively similar .  The most important question is if they had in
uterine tachysystole, what percentage went on to develop neonatal depression.  As you can see that it’s around 1.0% to 1.7%.  So, what is different
about those patients?  Why did they get into trouble?  Well, some patients tolerate uterine tachysystole much less well than others.
In this graph we’re looking at the average number of decelerations in the vertical column compared to how many contractions they were having.  So, as contractions per 10 minutes became more frequent, as we move to the right you can see that the number of deceleration also increases.  But was is very dramatic
here is that the babies with neonatal depression at almost every level of contractions have more decelerations.  That is, their compensatory capacity was less, they tolerated uterine tachysystole very poorly. You can see when they’re up around six and seven contractions, they have a lot of deceleration compared to the green, the normal, but they also had more deceleration at almost every level of contractions.
This is just another way of looking at rates of uterine tachysystole.  Here we’re looking at the rate not for the group in general as a whole, but at particular points in labor.  As we move towards the right we’re getting closer and closer to birth.   You can see the green for babies with normal gases at birth, rates of uterine tachysystole are quite low and they gradually increase as we get close to delivery.  For the babies with base deficits over twelve they also increased but much more  just before birth.  If we look at their response, this graph shows that response in the number of deceleration per contractions over time.  The babies in green tolerate their contractions quite well.  They do tend to have more deceleration per contractions because the contractions are stronger and they’re often more frequent as we get close to birth.  But the babies with metabolic acidemia have many more contractions and they do that for a long period of time.
In the red here are babies who not only have acidosis but also developed encephalopathy, seizures etc after birth.  You can see that they have an even more exaggerated response to contractions.  So, decelerations are very key consideration when you’re looking at the baby’s response to contractions.
In summary, uterine tachysystole is relatively common with the usual range of around 11 – 26%.  It’s usually short-lived.  How a baby responds to uterine tachysystole depends upon its balance between contraction-related decreases in profusion and the compensatory capacity of the baby.  Most babies have good
compensatory capacity, however it’s not unlimited.  Compensatory capacity is finite.  Red flags to look for are what is the deceleration response to any level
of contractions and also to consider what’s causing the UT.   Why?  Well, if it’s related to oxytocin, that’s relatively easy to correct.  Stop the oxytocin.  With a short half-life, it’s gone pretty much in a few minutes and the baby should recover whereas if the underlying cause is one of those things such as cardioamnitis or
an abrupted placenta that’s different.  With abruption we can’t modify its course and it may deteriorate very quickly.  So, we’ll always consider what’s causing it as well as what can we do about it.
Now we have some interesting case presentations and so I’m going to pass this back to Michelle and we’re going to go over four different cases.
Michelle Flowers:  Thank you Dr. Hamilton
As we begin our review of some cases here, we would like to acclimate you to the strip you’re seeing.  Across the top here you will see at 30 minutes  of tracing that includes a fetal heart rate and contraction.  Directly below this tracing, you’ll see a four-hour condensed view.  At the very bottom, is a persistent
contractility index with markings at 0, 15 and 30 respectively.  The orange markings signify tachysystole being detected.  There is a small magnifying slider window to the far right of this tracing and that portion within that window is the 30-minute tracing you’re seeing displayed across the top.
That being stated, let’s take a look at this first case.  This is a G3P1 thirty-nine and 5/7 weeks female.  Our compressed view here shows a four hour trend beginning at approximately 11:30 and starting to show a period of tachysystole that starts at right at 12:45.  We begin our review state here at the top at about 15:54.  We show that we have some variability present and as you look to the right, we see that there’s some decels here with our contractions.  You can see
that we start pushing about mid of that upper strip with a delivery resulting at about 15:22.  As we reviewed this strip, we can tell this infant was able to maintain a normadocic state delivering with a pH of 7.35 and a base deficit of o.6 with a resulting Apgar of eight and nine.  As we review the strip, you can tell this baby was able to accommodate a two and a half hour period of tachysystole.  Again, across the bottom, you can see this orange period where that tachysystole started right at that 12:45 mark, but due to the compensatory mechanisms and the fetal reserve of this infant it was able to tolerate.  We see it was decelling with the contractions, but it maintained its variability and again was able to deliver normadotic with Apgars of eight and nine.
Let’s take a look at our next case. This is four hours before delivery.  As you can tell, your slider window here at the beginning of that four hour compressed view.  This view began at about 19:00 so if we look across the top here it starts at 19:08 and ends at 19:28.  You can see that there’s some variability present and that we’re decelling towards about mid strip to the end.  We’re decelling with the contractions.  We’ve got about an hour of tachysystoly depicted across the bottom shown in the compressed view beginning at about 12:00 going through about 21:00.  It looks like it corrected for a little bit for a 30 minutes time-frame or so and then started again at about 21:45 into a tachysystolic state.  If we continue to look and we move our slider window to the end of the strip right here at delivery and look across the top, let’s see what we find now.  Again at about 21:45 where that sustained tachysystolic state continued at approximately at the top 22:28 and going through to 22:56 we see these decels with every contraction.  The baseline decreases at about 21:39 and the decels begin to get a little deeper and wider with a more smooth pattern.   So the smoother baseline looks like it’s beginning to lose some of its variability.  More importantly, they are getting wider and deeper with each contraction, falling at the end of the contractions even.
So it’s been in a period of tachysystole for roughly two and a half hours, with that one little break where it tried to recover, but then a sustained hour-and-a-half of tachysystole with the resulting vaginal delivery pH of 7.04 and a base deficit of 13.3.  However, it was able to have Apgars of 8 and 9 demonstrating it was able to compensate. But this compensatory compensatory capacity is finite.  We would consider this a near-miss.  The patient sustained a tacysystolic state for about two and a half hours or at least sustained for an hour and a half delivering with that 7.04 even though it was 8 and 9 Apgars, one would have hoped we could have intervened and space those contractions out, allowing this baby to have a rest in between to recover from the the contractions coming so rapidly back-to-back.
Now, let’s go on and look at our case number three.  Again, our slider bar magnification windows here at the end, right at delivery.  This is a G3P1 39 and 3/7 weeks.  We can see that our compressed view began and we are looking at our tachysystole beginning at about 15:00 and lasting through about 16:30 where it tries to correct it for a brief time and then started again at 173:0 with a resulting delivery at 18:54.  If we look across the top here at this last 30 minutes of strip, we see our baseline has started to be in a tachycardic state at 180 with decels at every contraction.  Rapid deterioration there right at delivery. Tachysystole was sustained for about an hour and a half  It’s the resulting pH a 7.05 and a base deficit of 16.2 but yet again the baby was able to compensate and deliver without Apgars 8 and 9.  This is yet another example of what we would consider to be a near miss.  The goal would have been to implement some interventions that could have spaced these contractions out and perhaps allow this baby to recover a bit prior to delivery or to expedite that delivery if it hadn’t have been the case.
Our final case presentation is another example of tachysystole and a resulting pattern.  So, with this one the strip started at 19:00.  This is a G1P0 39 and 0/7 weeks.  Our tachysystole began at about 21:15 and tries to auto correct a bit, then got persistent at 21:45.  The end of this particular strip segment is 22:47.  This
is right at about one and a half hours of sustained tachysystole with a resulting pattern as you see depicted.  These are considered deep and wide decels with a smooth baseline.  This would be an ominous pattern.  This would be one of those that just has no determinable baseline.  These are deep, wide, with every contraction.  You have no variability that can be spoken of and truly this would be one of the most ominous that we would come across.  So, in reviewing this resulting pH of 6.6 with a base deficit of 27 and resulting Apgar’s of zero and zero.
To sum up, recognizing tachysytolic patterns and beginning our interventions exponentially, then calling for assistance as needed and knowing when to escalate as appropriate for our unit protocol is of the most importance.  With that being stated, I would like to hand the presentation back to Dr. Emily Hamilton so we can now discuss the medical legal perspective of uterine tachysystole.
Dr. Emily Hamilton:   Thank you.  We have a few slides here to show some experiences with the medical legal aspects.
First, a number of studies.  All a little bit different, mostly looking at oxytocin use and uterine tachysystole and adverse outcomes.  These studies all come from different places in the world and they’re all showing more or less the same thing:  That with severe brain-related injury, like that last case that Michelle just decribed, rates of oxytocin misuse, uterine tachysystole, and delayed reaction to the tracing are very prevalent.
Now, one of these studies by Dr. Johnson in fact provides quite a bit of information comparing different subtleties about this subject in both the metabolic  acidosis group and in normal.  So we’ll look at that one in a little bit more detail.  The definition of UT here is a little bit different from what we use in North
America.  It’s greater than or equal to six contractions for 10 minutes lasting at least 20 minutes.  It’s similar, but not identical.  And what did they find? Well, they found oxytocin misuse in about 47%, almost half, of the babies with severe metabolic acidosis.  But oxytocinmisuse don’t necessarily mean uterine tachysystole.  It may mean simply increasing or failing to decrease oxytocin at the rate specified in a protocol.  But when they separated out how many actually had UT it was about 19% and as we’ve mentioned before uterine tachysystole may occur in the absence of oxytocin for other reasons and, in fact, you can see there’s an additional 7% who had uterine tachysystole, but without oxytocin.  So, overall, about a quarter of the babies with severe metabolic acidosis, seeking
legal action,  had uterine tachysystole.  That’s a very substantial proportion.
They too looked at a group that were normal and look for these same things.  You can see the same color coding here of oxytocin with uterine tachysystole at 3.2%. Uterine tachysystole without oxytocin misuse at 3.7%.  So, in total, about 7% of normal patients would have uterine tachysystole and they did just fine.  You can understand why people become blasé about uterine tachysystole.  We have to remember, not every baby can tolerate that.  There’s really no excuse for causing it and if you get to those babies with very bad birth-related injuries, that problem is very prevalent.
I am going to pass it back now to you, Michelle, for a few final conclusions.
Thank you so much Dr. Hamilton.  In conclusion, we know that fetal tolerance is demonstrated by changes in the fetal heart rate.  Our ability to recognize a decreasing variability or changes in baseline and decels is extremely important in our labor management.  Understanding the potential underlying cause and the appropriate interventions to take to correct is critical.  Knowing to turn the patient to her side, begin the O2, initiate the IV bolus, call for an assist,  discontinue the pitocin if in use or expedite labor if one of the other underlying causes for tachysystole have been identified.  All play critical parts.  Utilizing all the tools at our disposal to ensure we are aware of changes in the fetal heart rate and contraction pattern in order to intervene rapidly prior to the fetus exceeding its reserve  capacity can all have a tremendous impact on outcome.  We also realize that uterine tachysystole and the failure to intervene for abnormal fetal heart rate is very common in OB litigation.  So, again recognizing this pattern, assessing the cause and initiating appropriate intervention, calling for assist, and then
escalating as appropriately, all play critical roles.  We can even use the R-A-C-E acronym to help remember.  Oxytocin management protocols and checklist are helpful as well.  Documenting appropriately all the measures we have taken to correct the pattern is very important.  And, finally, avoiding the tachysystole.  Stopping our iatrogenic causes such as the oxytocin; expediting labor for those if it is a suspected abruption; employing the proper interventions for the probable underlying cause because ultimately failure to do so is indefensible.
Thank you very much for your participation today.  We hope it’s been helpful and helped in reminding us of some of our physiology the appropriate interventions.  We look forward to seeing you in future presentations.

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