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The nomenclature most commonly used in the United States is based on the timing of the deceleration in relation to contractions-thus treatment dynamics florham park buy cheap oxytrol on-line, early bad medicine 1 discount oxytrol 2.5mg otc, late hair treatment purchase oxytrol once a day, or variable medicine 8 discogs purchase cheap oxytrol line. In early and late decelerations, the slope of fetal heart rate change is gradual, resulting in a curvilinear and uniform or symmetrical waveform. With variable decelerations, the slope of fetal heart rate change is abrupt and erratic, giving the waveform a jagged appearance. Another system now used less often to describe decelerations is based on the pathophysiological events considered most likely to underlie the pattern. In this system, early decelerations are termed head compression, late decelerations are termed uteroplacental insufficiency, and variable decelerations are cord compression patterns. Accelerations these are abrupt heart rate increases above the fetal heart rate baseline and defined by an onset-to-peak rise within 30 seconds (American College of Obstetricians and Gynecologists, 2017a). Its duration is 15 sec but <2 minutes from onset to baseline return (see Table 24-1). According to Freeman and coworkers (2003), accelerations most often occur antepartum, in early labor, and in association with variable decelerations. Proposed mechanisms for intrapartum accelerations include fetal movement, stimulation by uterine contractions, umbilical cord occlusion, fetal stimulation during pelvic examination, scalp blood sampling, and acoustic stimulation. These are virtually always reassuring and almost always confirm that the fetus is not acidemic at that time. As with beat-to-beat variability, accelerations represent intact neurohormonal cardiovascular control mechanisms linked to fetal behavioral states. Krebs and colleagues (1982) analyzed electronic heart rate tracings in nearly 2000 fetuses and found sporadic accelerations during labor in 99. Fetal heart rate accelerations during the first or last 30 minutes during labor, or both, were a favorable sign for fetal well-being. The absence of such accelerations during labor, however, is not necessarily an unfavorable sign unless coincidental with other nonreassuring changes. The chance of acidemia in the fetus that fails to respond to stimulation in the presence of an otherwise nonreassuring pattern approximates 50 percent (Clark, 1984; Smith, 1986). Early Deceleration this physiological response shows a gradual fetal heart rate decline and then return to baseline associated with a contraction. Freeman and associates (2003) defined early decelerations as those generally seen in active labor between 4 and 7 cm cervical dilation. In their definition, the degree of deceleration is generally proportional to the contraction strength and rarely falls below 100 to 110 bpm or 20 to 30 bpm below baseline. Such decelerations are common during active labor and not associated with tachycardia, loss of variability, or other fetal heart rate changes. Importantly, early decelerations are not associated with fetal hypoxia, acidemia, or low Apgar scores. Characteristics include a gradual decline in the heart rate with both onset and recovery coincident with the onset and recovery of the contraction. Head compression probably causes vagal nerve activation as a result of dural stimulation, and this mediates the heart rate deceleration (Paul, 1964). Ball and Parer (1992) concluded that fetal head compression is a likely cause not only of the deceleration shown in Figure 24-11 but also of those shown in Figure 24-12, which typically occur during second-stage labor. Indeed, they observed that head compression is the likely cause of many variable decelerations classically attributed to cord compression. Maternal pushing efforts (lower panel) correspond to the spikes with uterine contractions. Fetal heart rate deceleration (C) is consistent with the pattern of head compression shown in Figure 24-11. Deceleration (B), however, is "variable" in appearance because of its jagged configuration and may alternatively represent cord occlusion. Late Deceleration the fetal heart rate response to uterine contractions can reflect uterine perfusion or placental function. A late deceleration is a smooth, gradual, symmetrical decline in fetal heart rate beginning at or after the contraction peak and returning to baseline only after the contraction has ended. In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively. The magnitude of late decelerations is seldom more than 30 to 40 bpm below baseline and typically not more than 10 to 20 bpm. Myers and associates (1973) studied monkeys in which they compromised uteroplacental perfusion by lowering maternal aortic blood pressure. The interval or lag from the contraction onset until the late deceleration onset was directly related to basal fetal oxygenation. They demonstrated that the length of the lag was predictive of the fetal Po2 but not fetal pH. The lower the fetal Po2 before contractions, the shorter the lag to the onset of late decelerations. This lag reflected the time necessary for the fetal Po2 to fall below a critical level necessary to stimulate arterial chemoreceptors, which mediated the decelerations. Characteristics include gradual decline in the heart rate with the contraction nadir, and recovery occurring after the end of the contraction. The nadir of the deceleration occurs 30 seconds or more after the onset of the deceleration. Murata and coworkers (1982) also showed that a late deceleration was the first fetal heart rate consequence of uteroplacental-induced hypoxia. During the course of progressive hypoxia that led to death over 2 to 13 days, monkey fetuses invariably exhibited late decelerations before development of acidemia. Generally, any process that produces maternal hypotension, excessive uterine activity, or placental dysfunction can induce late decelerations. The two most common sources are hypotension from epidural analgesia and uterine hyperactivity from oxytocin stimulation.
Thus medications via g tube purchase 5 mg oxytrol overnight delivery, variable decelerations represent fetal heart rate reflexes that reflect either blood pressure changes due to interruption of umbilical flow or changes in oxygenation symptoms your dog has worms buy oxytrol 5mg on line. It is likely that most fetuses have experienced brief but recurrent periods of hypoxia due to umbilical cord compression during gestation medications ibs buy oxytrol 2.5mg with amex. The frequency and inevitability of cord occlusions undoubtedly have provided the fetus with these physiological mechanisms as a means of coping medications vertigo buy generic oxytrol 2.5 mg on line. The great dilemma for the obstetrician in managing variable fetal heart rate decelerations is determining when variable decelerations are pathological. According to the American College of Obstetricians and Gynecologists (2017a), recurrent variable decelerations with minimal-to-moderate beat-to-beat variability are indeterminate, whereas those with absent variability are abnormal. Other fetal heart rate patterns have been associated with umbilical cord compression. The pattern consists of rapidly recurring couplets of acceleration and deceleration causing relatively large oscillations of the baseline fetal heart rate. We also observed a relationship between cord occlusion and the saltatory pattern in postterm pregnancies (Leveno, 1984). In the absence of other fetal heart rate findings, these do not signal fetal compromise. Lambda is a pattern involving an acceleration followed by a variable deceleration with no acceleration at the end of the deceleration. Prolonged Deceleration this pattern, which is shown in Figure 24-20, is defined as an isolated deceleration 15 bpm that lasts 2 minutes but <10 minutes from onset to return to baseline. Prolonged decelerations are difficult to interpret because they are seen in many different clinical situations. Some of the more frequent causes are cervical examination, uterine hyperactivity, cord entanglement, and maternal supine hypotension. Approximately 3 minutes of the tracing are shown, but the fetal heart rate returned to normal after uterine hypertonus resolved. Epidural, spinal, or paracervical analgesia may induce a prolonged deceleration (Eberle, 1998). Hill and associates (2003) observed prolonged deceleration in 1 percent of women given epidural analgesia during labor at Parkland Hospital. Other causes of prolonged deceleration include maternal hypoperfusion or hypoxia from any cause, placental abruption, umbilical cord knots or prolapse, maternal seizures including eclampsia and epilepsy, application of a fetal scalp electrode, impending birth, or maternal Valsalva maneuver. In one example, Ambia and colleagues (2017) described prolonged decelerations lasting 2 to 10 minutes following an eclamptic seizure. The placenta is effective in resuscitating the fetus if the original insult does not recur immediately. Occasionally, such self-limited prolonged decelerations are followed by loss of beat-to-beat variability, baseline tachycardia, and even a period of late decelerations, all of which resolve as the fetus recovers. Freeman and colleagues (2003) emphasize that the fetus may die during prolonged decelerations. Management of isolated prolonged decelerations is based on bedside clinical judgment, which inevitably will sometimes be imperfect given the unpredictability of these decelerations. Fetal Heart Rate Patterns During Second-Stage Labor Decelerations are virtually ubiquitous during the second stage of labor. Both cord and fetal head compressions have been implicated as causes of decelerations and baseline bradycardia in this stage. Profound, prolonged fetal heart rate deceleration in the 10 minutes preceding vaginal delivery has been described (Boehm, 1975). And, similar prolonged second-stage decelerations were associated with a stillbirth and neonatal death (Herbert, 1981). These experiences attest to the unpredictability of the fetal heart rate during second-stage labor. Spong and associates (1998) analyzed the characteristics of second-stage variable fetal heart rate decelerations in 250 deliveries. They found that as the total number of decelerations <70 bpm increased, the 5-minute Apgar score decreased. Of other patterns in second-stage labor, Picquard and coworkers (1988) reported that loss of beat-to-beat variability and baseline fetal heart rate <90 bpm predicted fetal acidemia. Krebs and associates (1981) also found that persistent or progressive baseline bradycardia or baseline tachycardia was associated with lower Apgar scores. Gull and colleagues (1996) observed that abrupt fetal heart rate deceleration to <100 bpm associated with loss of beat-to-beat variability for 4 minutes or longer was predictive of fetal acidemia. Thus, abnormal baseline heart rate-either bradycardia or tachycardia, absent beat-to-beat variability, or both-in the presence of deep second-stage decelerations is associated with a greater risk for fetal compromise. Admission Fetal Monitoring in Low-Risk Pregnancies With this approach, women with low-risk pregnancies are monitored for a short time on admission for labor. In one study, 3752 low-risk women in spontaneous labor at admission were randomly assigned either to auscultation of the fetal heart or to 20 minutes of electronic fetal monitoring (Mires, 2001). Moreover, its use resulted in a greater number of interventions, including operative delivery. More than half of the women enrolled in these studies eventually required continuous monitoring. A review by Devane and associates (2017) found that admission fetal monitoring programs for low-risk pregnancy are associated with a higher risk for cesarean delivery. Somewhat related, with the increasing rate of scheduled cesarean deliveries in the United States, clinicians and hospitals must decide whether fetal monitoring is required before the procedure in low-risk women. Computerized Interpretation Fetal heart rate pattern interpretations are subjective.
Etiopathogenesis To provide blood gas exchange immediately following delivery 5 medications that affect heart rate order cheap oxytrol online, the lungs must rapidly fill with air while being cleared of fluid medications 4 less canada buy oxytrol 5 mg otc. Although some of the fluid is expressed as the chest is compressed during vaginal delivery medicine merit badge order oxytrol cheap online, most is absorbed through the pulmonary lymphatics via complex mechanisms described in Chapter 32 (p treatment zoster ophthalmicus purchase oxytrol 2.5 mg with amex. It lowers surface tension and thereby prevents lung collapse during expiration (Chap. Although respiratory distress syndrome is generally a disease of preterm neonates, it does develop in term newborns, especially with sepsis or meconium aspiration. In these cases, surfactant can be inactivated by inflammation and/or presence of meconium (Chap. With inadequate surfactant, alveoli are unstable, and low pressures cause collapse at end expiration. Partial persistence of the fetal circulation may lead to pulmonary hypertension and a relative right-to-left shunt. When oxygen therapy is initiated, the pulmonary vascular bed dilates, and the shunt reverses. Protein-filled fluid leaks into the alveolar ducts, and the cells lining the ducts slough. Hyaline membranes composed of fibrin-rich protein and cellular debris line the dilated alveoli and terminal bronchioles. At autopsy, with hematoxylin-eosin staining of lung tissue, these membranes appear amorphous and eosinophilic, like hyaline cartilage. Because of this, respiratory distress syndrome is also termed hyaline membrane disease. Shunting of blood through nonventilated lung contributes to hypoxemia and to metabolic and respiratory acidosis. The chest radiograph shows a diffuse reticulogranular infiltrate and an airfilled tracheobronchial tree-air bronchogram. Although hypoxemia prompts supplemental oxygen, excess oxygen can damage the pulmonary epithelium, retina, and other immature tissues. Despite this, advances in mechanical ventilation technology have improved neonatal survival rates. This allows high inspired-oxygen concentrations to be reduced, thereby minimizing its toxicity. Namely, mechanical ventilation places a newborn at risk for barotrauma and volutrauma. In affected newborns, alveolar and pulmonary vascular development is disrupted and leads to hypoxia, hypercarbia, and chronic oxygen dependence (Davidson, 2017; Kair, 2012). The American Academy of Pediatrics now recommends against routine steroid use because of limited benefits and greater rates of impaired motor and cognitive function and school performance in exposed neonates (Doyle, 2014a,b; Watterberg, 2010). Despite initial enthusiasm, clinical trials failed to demonstrate a consistent benefit. Caffeine has been used widely to treat apnea of prematurity, but it also has bronchodilatory effects. The antioxidant vitamin A is necessary for normal lung growth and the integrity of respiratory tract epithelial cells. They contain biological or animal surfactants such as bovine-Survanta, calf -Infasurf, or porcine-Curosurf. Synthetic surfactants such as first-generation Exosurf and second-generation Surfaxin R are equivalent but not superior to animal-derived surfactant (Moya, 2007). In a Cochrane review, Ardell and coworkers (2015) found that animal-derived surfactants led to better outcomes than synthetic surfactants, which do not contain important surfactant proteins. It has been used for prophylaxis of preterm, at-risk newborns and for rescue of those with established disease. Given together, antenatal corticosteroids and surfactant result in an even greater reduction in the overall death rate. Exploration of different, less invasive ways to deliver rescue surfactant to spontaneously breathing preterm neonates is currently underway. Potential routes include surfactant application into the pharynx, surfactant nebulization, or application via laryngeal mask or via a thin catheter placed in the trachea (Kribs, 2016). The American College of Obstetricians and Gynecologists (2016a) considers all women at risk for preterm birth in this gestational-age range to be potential candidates for therapy. Amniocentesis to Assess Fetal Lung Maturity In some instances, when gestational age is uncertain, knowledge of fetal lung maturity may influence plans for delivery. One example is the woman with a prior classical cesarean delivery in whom repeat operation is planned and gestational age cannot be confirmed. Several tests are used to ensure fetal pulmonary maturity by analysis of amnionic fluid obtained by sonographically guided amniocentesis. At Parkland Hospital, we still find an occasional indication for such testing, however, the American College of Obstetricians and Gynecologists (2017a,b) counsels against its use in most of these cases. If amniocentesis is elected, fluid acquisition is similar to that described for second-trimester amniocentesis (Chap. Importantly, administration of corticosteroids to induce pulmonary maturation has variable effects on some of these tests. Of biochemical tests, the labor-intensive lecithin-sphingomyelin (L/S) ratio for many years was the gold-standard test. At 32 to 34 weeks, the concentration of lecithin relative to sphingomyelin begins to rise. Some recommend that phosphatidylglycerol, another surfactant phospholipid, be documented in amnionic fluid of these women.
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