What may be the cause of early decelerations while in labor?

Late Decelerations

The two varieties of late decelerations are reflex and nonreflex (Fig. 35.5).4,69–71Reflex late deceleration sometimes occurs when an acute insult (e.g., reduced uterine blood flow resulting from maternal hypotension) is superimposed on a previously normally oxygenated fetus in the setting of contractions. These late decelerations are caused by a decrease in uterine blood flow (with the uterine contraction) beyond the capacity of the fetus to extract sufficient oxygen. The relatively deoxygenated fetal blood is carried from the placenta through the umbilical vein to the heart and is distributed to the aorta, neck vessels, and head. The low Po2 is sensed by chemoreceptors, and neuronal activity results in a vagal discharge that causes the transient deceleration. The deceleration is presumed to be late because of the circulation time from the fetal placental site to the chemoreceptors and because the progressively decreasing Po2 must reach a certain threshold before vagal activity occurs. Baroreceptor activity also may cause the vagal discharge.69 Because oxygen delivery is adequate and there is no additional vagal activity between contractions, the baseline FHR is normal. These late decelerations are accompanied by normal FHR variability and signify normal central nervous system integrity (i.e., vital organs are physiologically compensated) (Fig. 35.6).

The second type of late deceleration results from the same initial mechanism except that the deoxygenated bolus of blood from the placenta is presumed to be insufficient to support myocardial action. For the period of the contraction, there is direct myocardial hypoxic depression (or failure) and vagal activity.69,71 These nonreflex late decelerations occur without FHR variability (Fig. 35.7), signifying fetal decompensation (i.e., inadequate cerebral and myocardial oxygenation). They are seen most commonly in states of decreased placental reserve (e.g., preeclampsia, intrauterine growth restriction) or after prolonged hypoxic stress (e.g., long period of severe reflex late decelerations).

Further support for the two mechanisms of late decelerations comes from observations of chronically catheterized fetal monkeys in spontaneous labor during the course of intrauterine death.72 The animals initially had normal blood gas values, normal FHR variability, FHR accelerations, and no persistent periodic changes. After various periods, they first demonstrated late decelerations and retained accelerations. This period was associated with a small decline in Po2 in the ascending aorta (28 to 24 mm Hg) and a normal acid-base state. These late decelerations were probably vagal reflex types caused by chemoreceptor activity. At an average of more than 3 days after the onset of these reflex decelerations, accelerations were lost in the setting of worsening hypoxia (Po2 = 19 mm Hg) and acidemia (pH = 7.22). Fetal death followed an average of 36 hours of persistent late decelerations without accelerations, which were presumed to be nonreflex decelerations associated with myocardial depression.

Decelerations

Decelerations are transient episodes of slowing of the FHR below the baseline level. The frequency with which they are found in normal antepartum records depends again on definition. If very small downward deflections, which otherwise might be included in the baseline variability, are identified as decelerations, these can be shown to frequently follow accelerations in a rather systematic pattern (Dawes et al., 1981a). In practice, decelerations are those downward deviations which are clearly distinct from the baseline variability. Thus in a study of normal fetuses during late pregnancy, the results of which are shown in Table 3, decelerations related to uterine contractions were found by Rüttgers et al. (1972) in 40% of the fetuses (n = 39), or in 11% of the 182 CTGs and in 28% of those with contractions. They were mostly (in 7% of the CTGs) of the mild, variable type, occurring in a nonrecurrent way with occasional contractions. Nonrecurrent contractions related to sporadic movement and causing mild variable decelerations may be part of a normal antepartum record.

Table 3. Incidence of Decelerations in Uncomplicated Late Pregnancy

Source: From Rüttgers et al. (1972).

Late decelerations have been shown by various investigators, and most recently by Parer et al. (1980), to be hypoxic in origin and thus abnormal. In 10% of fetuses with a normal pregnancy outcome, occasional but nonrecurrent late decelerations were seen. This evidence, presented in Table 3, suggests that occasional late decelerations without other adverse FHR characteristics are not a cause for intervention, although they cannot be regarded as completely harmless.

Repetitive and persistent late decelerations, on the other hand, should be regarded as a reliable sign of fetal hypoxia. They constitute, together with loss of variability, the major component of the diagnosis of antepartum fetal hypoxia (Hammacher, 1966; Kubli et al., 1972; Emmen et al., 1975) (Table 4). Marked and atypical contraction-related variable decelerations have the same significance as late decelerations (Kubli et al., 1972; Kubli et al., 1978; Visser et al., 1980) (Figure 2). Acute hypoxia such as occurs commonly with maternal supine hypotensive syndrome results in marked decelerations.

Table 4. Incidence of Decelerations with Antepartum Fetal Death

Source: From Kubli et al. (1972).

Decelerations

Decelerations in FHR are episodic decreases below the baseline. Most decelerations are mediated through parasympathetic stimulation from the vagal nerve. These, in turn, are triggered by a variety of stimuli, including transient increases in intracranial pressure (“early” decelerations), increased systemic vascular resistance (“variable” decelerations), and hypoxemia (some “late” decelerations). Thus, most decelerations do not specifically signify the presence of fetal acidosis, and in fact many are simply interesting demonstrations of human physiologic reflexes. A portion of “late” decelerations, however, occurs secondary to the suppression of myocardial function by tissue-level hypoxia, which is clinically concerning. Clinically differentiating these from other deceleration patterns, however, is often imprecise.

Decelerations are classified by their morphology and then by whether they are recurrent or prolonged. Decelerations are defined as “recurrent” if they occur with at least 50% of the contractions. A “prolonged” deceleration is one that lasts for more than 2 minutes. Three types of decelerations are described: early, variable, and late. Early decelerations are shallow and symmetric, gradual in onset and recovery, and associated with a contraction such that the nadir of the deceleration occurs at the same time as the peak of the contraction (Fig. 12.5). Physiologically, early decelerations are a demonstration of Cushing reflex, in which increased intracranial pressure generates bradycardia through stimulation of the vagal nerve. Because of the unfused cranial fontanelles, pressure applied to the fetal cranium, such as when the head is pressed against maternal tissue during a contraction, is translated into increased intracranial pressure and can trigger activation of the vagal nerve. Like most reflexes, the response is virtually instantaneous and the magnitude of vagal nerve stimulation correlates with the magnitude of pressure applied against the fetal head. This is why “early” decelerations appear as mirror images of the contractions. This entire process is unrelated to fetal oxygenation and acid-base balance, which is why early decelerations, although conceptually interesting, are not of clinical importance.

Variable decelerations are typically associated with an abrupt onset and abrupt return to baseline. They vary in shape, depth, and duration and in the occurrence of contractions. They are also frequently preceded and followed by small accelerations in FHR (Fig. 12.6 andFig. 12.7). Variable decelerations are usually associated with compression of the umbilical cord and represent physiologic changes in response to alterations in vascular resistance and preload. The umbilical cord contains a single large, thin-walled vein and two smaller, muscular arteries. When the umbilical cord is initially compressed, the umbilical vein is thus occluded first. This causes a decrease in venous blood returning to the fetal heart and, thus, a decrease in preload, which in turn triggers tachycardia. This is why variable decelerations are often preceded and followed by small increases in FHR, referred to colloquially as “shoulders.” As increasing compressive force is applied to the umbilical cord, the muscular arteries are eventually compressed as well. This then leads to a significant increase in vascular resistance, which in turn generates bradycardia via vagal nerve stimulation via baroreceptors. Although variable decelerations can sometimes occur normally during the labor process or even antenatal testing, their presence should alert the practitioner to the potential presence of umbilical cord compression, causes for which could include low amniotic fluid (oligohydramnios) or prolapse of the umbilical cord through the cervix. Overall, variable decelerations represent anticipated physiologic reflexes to umbilical cord compression and not the presence of hypoxemia or acidemia per se. However, severe and repetitive compression will eventually compromise oxygenation and overall health, and thus interventions (which can be as simple as maternal positional changes) would be warranted in this circumstance. Additionally, some fetuses can develop hypoxemia during periods of umbilical cord compression, which then normalizes after the compression is released. This can present as a period of tachycardia that follows resolution of the variable deceleration, owing to a sympathetic response to the hypoxemia. These are referred to as “overshoots” (seeFig. 12.7).

16 What are the mechanisms of injury to the thoracic great vessels?

Deceleration and traction are the most common mechanisms of injury to the thoracic arteries. Sudden horizontal deceleration creates marked shearing stress at the aortic isthmus (i.e., the junction between the mobile aortic arch and the fixed descending aorta) (see Fig. 71.1), whereas vertical deceleration displaces the heart caudally and pulls the ascending aorta and the innominate artery. Rapid extension of the neck or traction on the shoulder can also overstretch the arch vessels and produce tears of the intima, disruption of the media, or complete rupture of the vessel wall, leading to bleeding, dissection, thrombosis, or pseudoaneurysm formation. Aortic rupture leads to immediate hypovolemic shock and death in the vast majority of cases.

Decelerations

Decelerations include early, late, or variable decelerations.Early decelerations occur simultaneously with uterine contractions and usually are less than 20 bpm below baseline. The onset and offset of each deceleration coincides with the onset and offset of the uterine contraction (seeFig. 8.3). In animal models, head compression can precipitate early decelerations.36 In humans, early decelerations are believed to result from reflex vagal activity secondary to mild hypoxia. Early decelerations are not ominous.

Late decelerations begin 10 to 30 seconds after the beginning of uterine contractions, and end 10 to 30 seconds after the end of uterine contractions. Late decelerations are smooth and repetitive (i.e., they occur with each uterine contraction). Animal studies suggest that late decelerations represent a response to hypoxemia. The delayed onset of the deceleration reflects the time needed for the chemoreceptors to detect decreased oxygen tension and mediate the change in FHR by means of the vagus nerve.36,42 Late decelerations may also result from decompensation of the myocardial circulation and myocardial failure. Unfortunately, clinical and animal studies suggest that late decelerations may be an oversensitive indication of fetal asphyxia.36,39 However, the combination of late decelerations and decreased or absent FHR variability is an accurate, ominous signal of fetal compromise.39,43,44

Variable decelerations vary in depth, shape, and duration. They often are abrupt in onset and offset. Variable decelerations result from baroreceptor- or chemoreceptor-mediated vagal activity or possible transient hypoxemia.45,46 Experimental models and clinical studies suggest thatumbilical cord occlusion, either partial or complete, results in variable decelerations. During the second stage of labor, variable decelerations may result from compression of the fetal head. In this situation, dural stimulation leads to increased vagal discharge.47 The healthy fetus can typically tolerate mild to moderate variable decelerations (not below 80 bpm) without decompensation. With prolonged, severe variable decelerations (less than 60 bpm) or persistent fetal bradycardia, it is difficult for the fetus to maintain cardiac output and umbilical blood flow.47

Some practitioners additionally characterize decelerations as “atypical” when they demonstrate “shoulders,” “overshoot,” “biphasic” or “W pattern,” “slow return,” or absent variability at the nadir. The 2008 National Institute for Child and Human Development (NICHD) Consensus guidelines do not categorize atypical decelerations separately from other decelerations.35 There is controversy whether these atypical patterns indicate additional hazard for the fetus.48,49

Mitral Deceleration Time

Mitral DT is arguably the most important mitral variable for prognosis when heart disease is present, regardless of LVEF.21,32,94,95 In cardiac patients, mitral DT relates to LV chamber stiffness96; the shorter the mitral DT and the more “restrictive” the LV filling pattern, the higher the mortality.

The acceleration of E-wave mitral flow velocity is related to the maximum early diastolic transmitral pressure gradient. The deceleration of this flow, the mitral DT, is related to how fast (or slow) LV pressure increases in early diastole as volume enters the ventricle (the rapid filling wave as shown in Figs. 10-1 and 10-2). As with other mitral flow velocity variables, mitral DT changes with age, lengthening as the rate of LV relaxation slows and less volume is transferred to the ventricle in early diastole (see Table 10-1). A short mitral DT (140–160 msec) is normal in healthy, young individuals due to the high proportion of filling in early diastole that occurs because of LV elastic recoil. As E-wave velocity and the proportion of early diastolic filling declines with age, mitral DT increases to about 200 msec by age 65 (see Table 10-1).

With impaired LV relaxation and normal mean LA pressure, early diastolic filling is reduced (E/A wave ratio <1) and mitral DT is prolonged roughly in proportion to the slowing in the rate of LV relaxation.97 With pseudonormal mitral filling, the elevated mean LA pressure increases filling in early diastole into the noncompliant ventricle, and the rapid filling wave shortens the DT, with values that appear more normal for age. More advanced disease and further decreases in LV compliance cause such high LA pressure that blood is forced rapidly into a stiff ventricle in early diastole, which causes a very rapid, abnormal rise in LV pressure.19 A short mitral DT (<140 msec) characterizes this restrictive filling, which is most commonly seen in advanced dilated or restrictive cardiomyopathies. In these cases, and despite the widely variable LVEFs, mitral DT is strongly related to both the elevated filling pressures51 and survival.21,94

Mitral DT is dynamic and will change with alterations in preload and afterload that change the transmitral pressure gradient. Patients who are volume overloaded may lengthen their DT with diuresis. Similarly, mitral DT may lengthen and become less restrictive in response to a Valsalva maneuver (see Fig. 10-7) that lowers preload.30 Persistence of a restrictive LV filling pattern in a cardiomyopathy despite a Valsalva maneuver or after maximum medical therapy is the most severe form of diastolic dysfunction (grade IV; Figs. 10-7, 10-8, and 10-10), an ominous prognostic sign that indicates a very high mortality.32

Mitral DT is also useful in patients with MR, where the well-adapted ventricle will retain a normal DT. Shortening of the mitral DT from expected normal values for age indicates increased ventricular stiffness and is a better indicator of myocardial pathology than is peak E-wave velocity (see Fig. 10-16).

22 What is the significance of fetal heart rate decelerations?

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Early decelerations in FHR are caused by head compressions (vagal stimulation), are uniform in shape, begin near the onset of a uterine contraction with its nadir at the same time as the peak of the contraction, and are benign.

Variable decelerations are caused by umbilical cord compression and are nonuniform in shape. They are abrupt in onset and cessation. The decrease is >15 beats/min. They last longer than 15 seconds but less than 2 minutes. Although they usually do not reflect fetal acidosis, repetitive variable decelerations can lead to fetal hypoxia and acidosis.

Late decelerations are caused by uteroplacental insufficiency. They are uniform in shape. The onset and return to baseline are gradual. They often begin just after the onset of a contraction, with their nadir and recovery after the peak and recovery of the contraction. These decelerations are associated with maternal hypotension, hypertension, diabetes, preeclampsia, or intrauterine growth retardation. These are ominous patterns and indicate that the fetus is unable to maintain normal oxygenation and pH in the face of decreased blood flow.

The treatment for nonreassuring neonatal heart rate changes involves administering oxygen to the mother, maintaining maternal blood pressure, and placing the parturient in the left uterine displacement position (Figure 59-1).

Early Type.

An early deceleration is one that begins with the onset of a contraction, reaches its peak with the peak of the contraction, and then returns to normal baseline levels as the contraction ends (see Fig. 17.13).191,216,249,250 These decelerations appear to be related to compression of the fetal head and are mediated by vagal input to the heart.251-253 The mechanism of this effect of head compression may relate to a transient increase in intracranial pressure with secondary hypertension and bradycardia through the Cushing reflex. Early decelerations are not associated with fetal hypoxia, as reflected in fetal acid-base measurements or in neonatal depression.191,224,254

Traumatic Aortic Injury

Brutal deceleration injuries to the chest, especially from motor vehicle accidents, may result in traumatic rupture of the thoracic aorta, often just distal to the left subclavian artery at the aortic isthmus (i.e., the slight constriction of the aorta at the point where the ductus arteriosus attaches).73 Many of these patients die immediately, but some present with an acute paraplegia.74 Still others have a chronic aortic aneurysm that may present years later with acute spinal cord ischemia or other neurologic symptoms. Some patients with traumatic aortic injury have a less critical condition (e.g., limited intimal flaps) and may not warrant immediate surgical treatment.75 Nevertheless, they will still need to be monitored closely for signs of progression that would prompt urgent intervention.75

Pearls & Considerations