New WatchChild Release 1.6.4 Now Available
We’re pleased to announce the newest release of WatchChild. The release is designed to enhance and improve documentation and workflow at the bedside. It’s the result of customer requests and suggestions. To review the key improvements for WatchChild 1.6.4, visit the PeriGen Customer Portal. Please note that registration is required.
The importance of longer EFM views
Labor and delivery clinicians use EFM to identify fetal intolerance to labor to guide intervention and prevent hypoxic fetal injury. This task requires not only assessing the past and current degree of tracing abnormality and but projecting what is likely to happen in the near future. There is good evidence that tracing abnormalities generally evolve over hours (1-3). In addition, intervention guidelines usually recommend evaluating fetal response to supportive interventions over 30 to 60 minutes before resorting to cesarean delivery (4, 5). Thus long term assessments are essential. Standard computerized displays provide views of only 8 -10 minutes of tracing. Short term “snapshot” views can contribute to a failure to appreciate duration of tracing abnormality and the likely evolution.
PeriCALM Checklist analyzes EFM tracings in a consistent fashion. Its displays show long term trends over several hours, color coding regions of abnormality according to the criteria set by the institution. Such displays help clinicians see if a problem is intermittent or persistent, improving or deteriorating, stable or changing rapidly. A view of EFM trends may assist with situational awareness and helps clinicians in acute care settings more accurately project what is likely to happen and institute appropriate care. Checklist techniques and methods are especially pertinent in acute care settings during night time work when large amounts of data must be processed by the care givers over many hours. (6,7)
1. Vintzileos AM, Smulian JC. Decelerations, tachycardia, and decreased variability: have we overlooked the significance of longitudinal fetal heart rate changes for detecting intrapartum fetal hypoxia? Am J Obstet Gynecol. 2016 Sep;215(3):261-4.
2. Elliott C, Warrick PA, Graham E, Hamilton EF. Graded classification of fetal heart rate tracings: association with neonatal metabolic acidosis and neurologic morbidity. Am J Obstet Gynecol. 2010 Mar;202(3):258.
3. Clark SL, Hamilton EF, Garite TJ, Timmins A, Warrick PA, Smith S. The limits of electronic fetal heart rate monitoring in the prevention of neonatal metabolic acidemia. Am J Obstet Gynecol. 2016 Oct 14. pii: S0002-9378(16)30872-9. doi: 10.1016/j.ajog.2016.10.009. [Epub ahead of print]
4. 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. Intrapartum management of category II fetal heart rate tracings: towards standardization of care. Am J Obstet Gynecol. 2013 Aug;209(2):89-97.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 106: Intrapartum fetal heart rate monitoring: nomenclature, interpretation, and general management principles. Obstet Gynecol. 2009 Jul;114(1):192-202.
6. Chapter 46. Fatigue, Sleepiness, and Medical Errors. AHRQ. (accessed December 2, 2016) https://archive.ahrq.gov/clinic/ptsafety/chap46a.htm
7. Fioratou E, Flin R, Glavin R, Patey R. Beyond monitoring: distributed situation awareness in anaesthesia. Br J Anaesth. 2010;105:83-90.
EFM Assessment Agreement & Standardization
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.
by Rebecca Cypher, MSN, PNNP
Chief Nursing Officer, PeriGen
I hope you enjoyed the first two excerpts from my recent white paper on technologies in perinatal nursing. This article, done on request by PeriGen (the electronic fetal monitoring software firm for which I serve as Chief Nursing Officer), looks at how technology has evolved in response to changes in perinatal nursing, how we in turn have changed as a result of electronic FHR monitoring, and a view to how we as nursing professionals can influence continued improvement in perinatal technologies.
Below is the final excerpt where we examine the importance of a perinatal nurses view on technology improvements. In case you missed the first two installments, PeriGen has posted the full article as a PDF here.
Why Should Nurses Care?
Between 2008-2012, there were 2.8 million registered nurses (including advanced practice nurses) in the United States workforce making nursing one of the largest health-related professional groups. 24, 29, 30 According to Gallup polls, these professionals are regarded by the public as the most trusted in the United States. Nursing is a caring profession that requires licensure, knowledge and clinical skill. Nursing demonstrates the best side of humanity. Well-designed HIT augments nursing capacity. Nurses must be clear in thinking and understanding the relative strengths and limitations of all parties in order to direct the evolution of these technologies. In turn, nurses can harness these technologies to support the mission of providing high quality patient care that is evidence-based, individualized, efficient and safe.
Government agencies expect a 21% increase in demand for nurses nationwide by 2025 though considerable variation of supply and demand at the state level is anticipated. Nursing employment will continue to be affected by factors including population growth, a shift in demographics as the median age increases, economic conditions, employment and retirement of nursing personnel and changes in health care reimbursement. Workforce projection models demonstrate that the rapidly changing health care delivery system, which includes HIT, is shifting how patient care is delivered and the specific role the nursing workforce plays in these changes. 31
Perinatal nurses are using technology in conjunction with clinical knowledge that has been accumulated through hands on experience and education. This combination assists in improving care and facilitates multidisciplinary communication. Technology allows nurses to ask the right questions at the right time, perform streamlined nursing assessments, accurately determine a correct diagnosis from a multidisciplinary approach, and perform appropriate tasks and intervention on the front and back end of decision-making processes. 32
In this modern era, technology is commonplace whether it’s embedded in households, communication methods, modes of transportation or healthcare. In these areas technology continues to be created, refined and updated on a regular basis. Advances in technology, whether it’s a new cellular phone model or component of medical equipment, are requisite in order to provide and improve efficiency, convenience, accessibility and safety. As nurses provide day to day quality patient care in the perinatal setting, technology will continue to influence many facets of the nursing process framework. In today’s healthcare environment, few perinatal nurses can envision delivering patient care without assistance from some form of technology, whether that technology be an automatic blood pressure machine or fetal surveillance with an electronic fetal monitor. Nursing is what we as individuals do best and nurses working in conjunction with HIT is clearly an investment in optimizing efficiency, perinatal outcomes and patient safety. Throughout time women in labor have sought assistance from others with experience and skills. Clearly nurses will continue to fill that essential role backed by increasingly complex technology as HIT evolves.
Now there’s a way to reduce
transcription, toggling, errors
with PeriCALM Data Export
PeriGen introduces the latest data integration improvement to PeriCALM® Patterns™ and PeriCALM® CheckList™: A data export feature designed to reduce time spent on transcribing EFM data and toggling between systems to capture and post it.
The new feature, the result of feedback received by a large number of labor & delivery clinicians at the 2015 AWHONN Convention, as well as current customers, was launched at PeriGen’s booth during the 2016 AWHONN Convention in Grapevine, TX.
How PeriCALM Data Export Works
Patterns and CheckList data export allows PeriCALM users to select 15- or 30-minute EFM summary information for posting into an annotation and, where enabled, designated EHR fields in real-time with just a few clicks of the mouse.
The new features adds an icon that activates selection of a specific section of tracing and generates an Export Dialog. The dialog automatically populates with a summary of FHR and uterine activity measurements for the specificed time range, as calculated by PeriCALM Patterns or CheckList.
This EFM data points are customizable and can include baseline, variability, the number and types of decels, etc. The feature also allows the user to modify each data point and add comments. Once reviewed and approved by the user, the data Export button sends the data to the tracing as an annotation. If the associated EHR is configured to accept this data, the same click can send it to the EHR with a time, date, and user stamp.
The feature is designed to provide real-time data while saving labor & delivery clinicians time that’s currently wasted on transcription, toggling between screens and systems, and cumbersome calculations better handled by computer.
In early tests of the new feature, one user found she saved 5 minutes an hour while charting. PeriGen will be conducting research to measure time-savings before and after the new data export feature is introduced at client hospitals.
Email firstname.lastname@example.org or contact your Client Executive to participate in these studies or see a demonstration of the new data export feature.
Are you using just data or rich clinical information to assess labor?
Here’s a definition of data
According to Merriam-Webster’s dictionary, data is the output from a sensing device that includes both useful and relevant or redundant information and must be processed to be meaningful.
Here’s a familiar example:
Traditional electronic fetal monitoring systems, developed long before computers made real-time analysis possible in a hospital setting, deliver numeric measurements of fetal heart rate and contractions and presents them in graph form.
Converting this obstetric data to information of actual use is left entirely up to clinicians in their role as human calculators.
Here’s a definition of clinical information
Knowledge obtained from investigation, study, or instruction which justifies change in a plan or theory.
Information-rich decision support tools, illustrated in the PeriCALM® screenshot shown above, convert data into intelligence that make more robust interpretation and decision-making possible.
How many perinatal nurses are limited to just using data to assess labor?
Which is of more use? How would having the rich clinical information shown above make a difference with your work?
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).
Wednesday, March 16th
Noon – 12:30 PM ET
Fetal Heart Rate Variability
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.
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.
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.
Late Fetal Heart Rate (FHR) Decelerations
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.
What Regulates the Fetal Heart Rate?
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.
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 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.