There are still a couple of spots open for tomorrow’s free online continuing education session covering uterine activity management.
Unfortunately, Rebecca Cypher, MSN, PNNP, PeriGen’s Chief Nursing Officer, originally scheduled to present tomorrow’s CE webinar, will not be able to make it. Michelle Flowers R, an AWHONN-certified continuing education instructor, will be leading the session instead supported by Dr. Emily Hamilton, PeriGen’s Senior Vice President of Clinical Research. They will be covering the nomenclature and definitions related to uterine activity, the etiology of uterine tachysystole (UT) and UT’s impact on FHR.
PeriGen has provided a date for the first in a series of free online continuing education webinars. The series, featuring Chief Nursing Officer Rebecca Cypher, MSN, PNNP, will offer educational topics related to fetal monitoring, patient safety, and multidisciplinary care in the perinatal setting. Sessions are intended to assist clinicians in translating and incorporating evidence-based information into daily clinical activities.
The first webinar will cover uterine activity and is scheduled for March 8th, noon – 1:00 PM ET. Titled “Power & Passenger: Understanding Uterine Activity,” this session is designed to examine nomenclature and definitions associated with uterine activity, etiologic principles of uterine tachysystole and tachysystole’s impact on fetal heart rate.
Last week’s presentation on EFM Assessment Agreement packed a lot into 30-minutes. Emily Hamilton, PeriGen’s SVP of Clinical Research reviewed the research related to low levels of agreement among even expert clinicians on core EFM feature assessments.
Emily then reviewed how modern technology has adapted to the problem of standardizing EFM analysis, making it easier for clinicians to see concerning trends and response to clinical interventions.
How many labor & delivery nurses NEVER ask for a second opinion when interpreting a tracing? If you do, is that a bad thing?We ask because it turns out that a fair amount of research says that labor nurses SHOULD ASK for a back up opinion. Multiple research studies show that agreement about FHR tracing interpretation is a pretty rare event.
Discover what this research tells us and how some of today’s leading OB clinicians are using technology tools to gain a valuable second opinion before they make important care decisions. Register for a free webinar on Sept. 28th, Noon – 12:30 PM ET
Sally has worked as a labor & delivery nurse for twelve years. Her team brags that she can interpret a strip from 15 feet away. Today she’s teamed up with Laura, a 3-year veteran, taking care of a high-risk mother in early labor.
While Sally’s taking lunch, Laura starts seeing some variable decels. She pulls up a new software program her hospital has provided, reviewing the last four hours of tracing to see if she can see a pattern of variability. Not yet, but she thinks it’s something to keep an eye on.
Before taking her own lunch break, she suggests that Sally keep an eye on the trend line shown in the new tool. Sally’s not sold on the new tool, so she continues to watch the shorter views, noting the decels and baselines with her experienced eyes.
On September 28th, from noon – 12:30 PM ET, learn how even the most experienced clinicians often disagree about the interpretation of FHR tracings and misjudge the duration of abnormality that can be highlighted by modern perinatal technology.
Here’s a summary of what Emily Hamilton, MDCM will be covering during tomorrow’s free perinatal nursing training webinar designed to help clinicians improve their ability to understand FHR variation and decelerations.
What regulates the fetal heart rate
Fetal heart rate decelerations
How they affect clinical interpretation of tracings
Perinatal Training Summary:
The clinical goal of electronic fetal monitoring is to identify fetuses with increased risk of hypoxic injury so that intervention can be executed to avoid adverse outcomes without also causing excessive number of interventions. Understanding the mechanisms of fetal heart rate control is important because it can help us to infer the physiological state of the baby and gauge whether intervention is truly necessary.
Unlike in adult cardiology, where ECG changes are used to diagnose myocardial infarction, labor & delivery clinicians depend upon the heart rate to infer the condition of another organ, namely the fetal brain. Although the fetal heart rate is related to fetal brain state, is is also affected by a number of other factors.
During tomorrow’s training webinar, Dr. Hamilton will provide an overview of recent perinatal research on these factors.
Registration is still open, but “seats” are filling fast
The following is this week’s excerpt from The Physiology of EFM. Hear author Emily Hamilton review the entire contents of this white paper during the free online training webinar designed for labor & delivery clinicians on March 16th (Noon – 12:30 PM ET).
Current clinical guidelines that classify tracings rely heavily on reduced baseline heart rate variability as an indicator of significant acidosis and/or need for intervention.6-12 Minimal variability, especially when it persists and is accompanied by decelerations, is associated with marked acidemia, low Apgar scores and hypoxic injury.
Minimal variability, especially when it persists and is accompanied by decelerations, is associated with marked acidemia, low Apgar scores and hypoxic injury.
All of the mechanisms controlling fetal heart rate depicted in Figure 1 influence heart rate variability. Fetal behavioral states, breathing and movements affect heart rate variability acting though the central pathways to the medulla, and then to the heart via the sympathetic and parasympathetic systems. Fetal heart rate variability is suppressed by factors that depress fetal brain function.
Animal experiments have shown that blockage of the parasympathetic system with atropine results in a reduction in short-term variability.13 A reduction in long-term variability occurs after sympathetic blockade.14, 15 Fetal heart rate variability is more than the simple “push-pull” interactions between the inhibitory and acceleratory limbs of the autonomic nervous system. The heart itself contributes to variability. Even with complete double blockade of the sympathetic and parasympathetic systems, around 35-40% of fetal lamb heart rate variability persists.13 A clinical demonstration of the intrinsic rhythmicity of the heart is found in transplantation surgery. An excised heart continues to beat and demonstrate heart rate variability.
Marked variability may be a sign of activation of compensatory pathways.
The association between variability and metabolic acidosis is less clear. This is important because all contemporary EFM classification methods place high reliance upon baseline fetal heart rate variability to exclude the presence of metabolic acidosis.6-12 The 2008 NICHD Update publication in which the Category I, II, III classification method was first described includes a statement that “moderate variability reliably predicts the absence of metabolic acidemia at the time that it is observed.”6 This concept was softened in the 2009 ACOG Practice Bulletin 106 with the statement “The data relating FHR variability to clinical outcomes, however, are sparse.”7 This practice bulletin endorsed the 3-level categorization of tracings where the third level required absent baseline variability.
The 2010 ACOG Practice Bulletin 116 presented a clinical management algorithm with high reliance on moderate variability.8 In this management algorithm, the recommendations for tracings in Category 2 were continued surveillance and intrauterine resuscitation measures, as long as there was moderate variability. Only a failure to respond to intrauterine resuscitative measures in the presence of absent or minimal variability lead to the recommendation of “consideration of delivery” for Category II tracings.
There is a growing body of literature that does not support the statement that moderate variability reliably excludes the presence of metabolic acidemia.
In animal studies, vascular instrumentation allows for blood gas measurement at any specific time to be correlated with the coexisting fetal heart rate features. Martin demonstrated that in sheep the initial fetal heart rate response to sudden hypoxemia was a slowing of the heart rate with increased variability.1 Others observed similar changes in sheep and in monkeys.16-18 Field et al found initial decreases in heart rate variability with iliac occlusion in sheep, but variability returned to normal by 36 minutes despite worsening metabolic acidosis.19 These observations of normal variability in the face of acidemia led researchers to postulate that some aspect of variability control could be different in animals compared to humans.
In the human literature, four recent and independent studies using various definitions of acidosis and examining the last 30-60 minutes of the tracing reported that the percentage of babies with acidosis who had moderate variability ranged from 15% to 91%.20-23 Even with near lethal levels of uterine artery base deficit (>=16 mmol/L), a full 15 to 32% of these babies had moderate baseline variability in the tracing recorded just before birth.20, 21 Another study examined baseline variability in term babies who required supplemental oxygen for more than 6 hours or mechanical ventilation.24 In this study, marked variability in the last 30 minutes was significantly associated with these respiratory morbidities. Minimal variability was not. This finding is in keeping with other direct observations on the correlation between increased heart rate variability and catecholamines concentration on non-acidotic term fetuses.25 It appears that marked variability may be a sign of activation of compensatory pathways.
The following excerpt is taken from The Physiology of EFM, a PeriGen white paper written by Emily Hamilton, MDCM and Philip Warrick, Ph.D. Its contents are among the topics to be covered at the free March 16th lunchtime labor & delivery training webinar.
Figure 3: Two pathways are involved with late decelerations, adapted from Martin 1979 (1) and Freeman et al. (2)
To simulate decreased uteroplacental oxygen delivery, Martin applied repeated hypogastric artery occlusions in sheep. These occlusions resulted in fetal hypertension which was followed by vagally mediated decelerations. The degree of hypertension and the amount of deceleration were closely related, although some deceleration remained when the transient hypertension was prevented by alpha-adrenergic blockade. The timing of the onset, nadir and end of the deceleration was delayed with respect to the occlusion and mirrored the timeline of the hypertensive response. Vagal blockade eliminated these decelerations in the non-acidemic sheep. Thus, “intermittent placental insufficiency” can cause decelerations and its effects are mediated by the vagus nerve. These “late” decelerations were not associated with fetal acidosis. 1, 3
When the occlusions were extended to produce fetal acidosis, the fetal hypertensive response lost its progressive character, reaching a plateau early after the beginning of the occlusion, while the deceleration continued to fall with its nadir occurring at or after the end of the occlusion. With progressive acidemia the decelerations became deeper and longer. In the presence of very severe acidemia (pH=6.96) they could not be eliminated by vagal blockade. With complete vagal and alpha and beta adrenergic blockade, the decelerations persisted. The fetal heart, devoid of any sympathetic and parasympathetic influences, showed decelerations suggesting that intrinsic myocardial depression was the deceleration mechanism in the presence of severe acidosis and hypoxia.3
Although the individual pathways described above cover the major mechanisms of fetal heart rate decelerations, the actual situation is more complex. Even in the sheep experiments using precisely controlled conditions, consistent fetal heart rate decelerations could not be produced equally in all animals despite 2 hours of repetitive maternal vascular occlusions.3
The following excerpt summarizing the factors regulating the fetal heart rate will be summarized in the free March 16th lunchtime L&D staff training webinar titled “The Physiology of EFM” featuring Emily Hamilton, MDCM.
The heart is a muscle with its own pacemaker, conducting system, numerous types of receptors (alpha and beta adrenergic) and direct neuronal connections to both the sympathetic and parasympathetic systems.
The overarching mission of the cardiovascular system is to deliver sufficient oxygen to key organs. Heart rate is an important determinant of this mission.
Ultimately, any influence on heart rate is mediated by one or more of these structures. The basic anatomy and physiology of heart rate control are described in physiology textbooks. In the simple schematic diagram shown in Figure 1, factors which increase heart rate are shown on the left and factors which decrease heart rate are on the right. While this summary provides the basics for understanding heart rate regulation, it is important to remember that our understanding of this physiology continues to evolve.
The cardioregulatory center in the medulla oblongata contains an acceleratory center and an inhibitory center. The cardioregulatory center receives input from the central nervous system, reflex pathways and circulating catecholamines. An example of central nervous system influence on the acceleratory response is seen with vibroacoustic stimulation. In response to sudden auditory stimulation, the central nervous system activates the cardioacceleratory center. The cardioacceleratory center increases heart rate directly via sympathetic cardiac nerves which interact with the sinoatrial node to increase the heart rate.
The rapidity of heart rate change is determined by the conditions that trigger the change.
The cardioinhibitory center slows the heart rate via the parasympathetic vagus nerve which can slow heart rate by modulation at various levels, including the sinoatrial node. Reducing cardioinhibitory activity increases heart rate.
Arterial baroreceptors, located in the aortic arch and carotid arteries, are sensitive to stretch or distension of a vessel caused by blood pressure changes. An increase in arterial blood pressure produces vessel distension and causes arterial baroreceptors to send neuronal messages to the cardioinhibitory center, which in turn causes rapid slowing of the fetal heart rate via the parasympathetic vagus nerve. A decrease in arterial pressure results in an increased heart rate.
Arterial chemoreceptors located in the aortic arch and carotid arteries are sensitive to low pH and low oxygen saturation. When these chemoreceptors are activated, they cause the cardioacceleratory center to increase sympathetic impulses, resulting in an increase in the fetal heart rate. The α-adrenergic component of the chemoreceptor response causes vasoconstriction and hypertension. As will be described later, hypertension is an important part of the pathway producing fetal heart rate decelerations.
The catecholamines, epinephrine and norepinephrine, secreted from the adrenal, are both hormones and neurotransmitters. Norepinephrine binds to beta receptors in the heart causing an increase in heart rate, contractility and stroke volume. Catecholamines can also cause redistribution of blood flow by inducing vasoconstriction and vasodilation in different regions. Vasoconstriction is mediated through the α-adrenergic receptors in liver, kidney, skin and gut, and vasodilation is mediated through β adrenergic receptors in skeletal muscle. Catecholamine release is stimulated by the sympathetic nervous system and may be precipitated by stress conditions, such as loud sounds, fear or low blood sugar.
The rapidity of heart rate change is determined by the conditions that trigger the change. Central stimuli like a sudden loud sound or a quick increase in blood pressure cause rapid heart rate changes mediated by direct neuronal pathways to the sinoatrial node. Although chemoreceptor action on heart rate is also mediated neuronally (by the cardiac nerves), this influence tends to be slow because it is triggered by low pH and oxygen levels which tend to fluctuate slowly. Catecholamine mediated effects are relatively slow reflecting their half-life of 2 to 3 minutes.
While all of the mechanisms described above modulate heart rate, it is important to recall that the overarching mission of the cardiovascular system is to deliver sufficient oxygen to key organs. Heart rate is an important determinant of this mission but only one, along with other cardiovascular compensatory mechanisms, which include redistribution of blood flow and changes in blood pressure, cardiac stroke volume or oxygen carrying capacity and hemoglobin-oxygen dissociation in the blood stream. The medulla oblongata contains the vasomotor center that responds to baroreceptors, chemoreceptors and catecholamines. It also regulates peripheral blood vessel dilation and constriction to help maintain normal blood pressure and distribution of blood to vital organs.
Last week’s webinar, covering research on a new method to assess labor progress, continues to stimulate comment and debate. The session described a whole new labor curve concept, one that adapts to the multiple factors affect dilation directly and change as labor advances. Recent peer reviewed publications report a five-fold improvement in the rate of identification of first time mothers who actually underwent a cesarean for slow labor using the PeriCALM Curve compared to the rate using the current fixed labor curves that are based on time only (70% vs 12%).
The research, outlined in two articles recently published in the American Journal of Obstetrics & Gynecology, was reviewed by Dr. Emily Hamilton during a lunchtime session offered by PeriGen. The session, titled “Rethinking the Labor Curve,” was recorded and can be viewed here.
Dr. Hamilton led the research team that applied a modern, mathematical approach to the assessment of labor. The team found that the utility of contemporary labor curves was limited because of, among other things, a wide degree of variation in the early stages of labor. In fact, it is not until late labor when dilation reaches six centimeters that this variation enters useful limits and the contemporary curves can be used. The new approach can be applied earlier to assess two essential processes for vaginal birth (dilatation and descent). Results are expressed with percentiles and graphs.