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  1. 1. Chapter 22Intrapartum Fetal Surveillance Michael P. Nageotte, MD, and Larry C. Gilstrap III, MD ability. Hence, there are two possible vagal influences on the heart: a tonic influence tending to decrease FHR and an oscillatory influenceFactors Controlling Fetal that results in FHR variability.2 Further, vagal tone is not necessarilyHeart Rate constant. Its influence increases with gestational age.3 In fetal sheep, vagal activity increases as much as fourfold during acute hypoxia4 orFetal heart rate (FHR) analysis is the most common means by which experimentally produced fetal growth restriction.5a fetus is evaluated for adequacy of oxygenation. Knowledge of the rateand regulation of the fetal heart is therefore of great importance to theobstetrician. At 20 weeks of gestation, the average FHR is 155 beats/ Sympathetic Nervous Systemmin; at 30 weeks, it is 144 beats/min; and at term, it is 140 beats/min. Sympathetic nerves are widely distributed in the muscle of the heartThis progression is thought to be related to maturation of vagal tone, at term. Stimulation of the sympathetic nerves releases norepinephrinewith consequent slowing of the baseline FHR. Variations of 20 beats/ and causes increases in both the rate and the strength of fetal cardiacmin faster or slower than these baseline values are present in normal contractions, resulting in higher cardiac output. The sympatheticfetuses. nerves are a reserve mechanism to improve the pumping activity of The fetal heart is similar to the adult heart in that it has its own the heart during intermittent stressful situations. There is normally aintrinsic pacemaker activity which results in rhythmic myocardial con- tonic sympathetic influence on the heart. Blocking the action of thesetractions. The sinoatrial node, found in one wall of the right atrium, sympathetic nerves causes a decrease in FHR of approximately 10has the fastest rate of conduction and sets the rate in the normal heart. beats/min. As with the vagal tone, tonic sympathetic influence increasesThe next fastest pacemaker rate is found in the atrium. Finally, the as much as twofold during fetal hypoxia.ventricle has a slower rate than either the sinoatrial node or the atrium.In cases of complete or partial heart block in the fetus, variations inrate markedly slower than normal can be seen. The rate in a fetus with Chemoreceptorsa complete heart block is often 60 to 80 beats/min. Chemoreceptors are found in both the peripheral and the central Variability of the FHR is important clinically and is of prognostic nervous system. They have their most dramatic effects on the regula-value with respect to its specific amplitude as part of the FHR pattern. tion of respiration but are also important in control of the circulation.The heart rate is the result of many physiologic factors that modulate The peripheral chemoreceptors are in the aortic and carotid bodies,the intrinsic rate of the fetal heart, the most common being signals which are located in the arch of the aorta and the area of the carotidfrom the autonomic nervous system. sinus, respectively. The central chemoreceptors in the medulla oblon- gata respond to changes in oxygen and carbon dioxide tension in the blood or in the cerebrospinal fluid perfusing this area.Parasympathetic Nervous System In the adult, when oxygen is decreased or the carbon dioxideThe parasympathetic nervous system consists primarily of the vagus content is increased in the arterial blood perfusing the central chemo-nerve (10th cranial nerve), which originates in the medulla oblongata. receptors, a reflex tachycardia occurs. There is also a substantial increaseThe vagus nerve innervates both the sinoatrial and the atrioventricular in arterial blood pressure, particularly when the carbon dioxide con-nodes. Stimulation of the vagus nerve results in a decrease in FHR in centration is increased. Both effects are thought to be protective, rep-the normal fetus, because vagal influence on the sinoatrial node resenting an attempt to circulate more blood through the affected areasdecreases its rate of firing. In a similar fashion, blockade of this nerve and thereby bring about a decrease in carbon dioxide tension (PCO2)in a normal fetus causes an increase in the FHR of approximately or an increase in oxygen tension (PO2). Selective hypoxia or hypercap-20 beats/min at term.1 This finding demonstrates a normally constant nia of the peripheral chemoreceptors alone in the adult produces avagal influence on the FHR, which tends to decrease it from its intrinsic bradycardia, in contrast to the tachycardia and hypertension thatrate. results from central hypoxia or hypercapnia. The vagus nerve has another very important function: It is respon- The interaction of the central and peripheral chemoreceptors in thesible for transmission of impulses causing beat-to-beat variability of fetus is poorly understood. It is known that the net result of hypoxiaFHR. Blockade of the vagus nerve results in disappearance of this vari- or hypercapnia in the unanesthetized fetus is bradycardia with hyper-
  2. 2. 398 CHAPTER 22 Intrapartum Fetal Surveillancetension. During basal conditions, the chemoreceptors contribute tostabilization of FHR and blood pressure.6 Blood Volume Control Capillary Fluid ShiftBaroreceptors In the adult, when the blood pressure is elevated by excessive bloodIn the arch of the aorta, and in the carotid sinus at the junction of the volume, fluid moves out of the capillaries into interstitial spaces,internal and external carotid arteries, are small stretch receptors in thereby decreasing the blood volume toward normal. Conversely, if thethe vessel walls that are sensitive to increases in blood pressure. When adult loses blood through hemorrhage, some fluid shifts out of thepressure rises, impulses are sent from these receptors via the vagus or interstitial spaces into the circulation, increasing the blood volumeglossopharyngeal nerve to the midbrain; this results in further impulses’ toward normal. There is normally a delicate balance between the pres-being sent via the vagus nerve to the heart, tending to slow it. This is sures inside and outside the capillaries. This mechanism of regulatingan extremely rapid response, occurring almost with the first systolic blood pressure is slower than the almost instantaneous regulationrise of blood pressure. It is a protective, stabilizing attempt by the body observed with the reflex mechanisms discussed previously. Its roleto lower blood pressure by decreasing the heart rate and cardiac output in the fetus is imperfectly understood, although imbalances may bewhen blood pressure is increasing. responsible for the hydrops seen in some cases of red cell alloimmu- nization and the high-output failure sometimes seen with supra- ventricular tachycardia.Central Nervous SystemIn the adult, the higher centers of the brain influence the heart rate. Intraplacental PressuresHeart rate is increased by emotional stimuli such as fear and sexual Fluid moves along hydrostatic pressure gradients and in response toarousal. In fetal lambs and monkeys, the electroencephalogram or osmotic pressure gradients. The specific role of these factors within theelectro-oculogram shows increased activity, at times in association human placenta, where fetal and maternal blood closely approximate,with increased variability of the FHR and body movements. At other is unclear. It seems likely, however, that some delicate balancing mecha-times, apparently when the fetus is sleeping, body movement slows and nisms within the placenta prevent rapid fluid shifts between motherFHR variability decreases, suggesting an association between these two and fetus. The mean arterial blood pressure of the mother (approxi-factors and central nervous system activity.7 mately 100 mm Hg) is much higher than that of the fetus (approxi- The medulla oblongata contains the vasomotor centers, integrative mately 55 mm Hg), but the osmotic pressures are not substantiallycenters in which the net result of all the inputs is either acceleration different. Therefore, some compensatory mechanism must be presentor deceleration of the FHR. It is probably in these centers that the to equalize the effective pressures at the exchange points so as tonet result of numerous central and peripheral inputs is processed prevent dramatic fluid shifts.to generate irregular oscillatory vagal impulses, giving rise to FHRvariability. Frank-Starling Mechanism The amount of blood pumped by the heart is determined by theHormonal Regulation amount of blood returning to the heart; that is, the heart normally pumps the blood that flows into it without excessive damming of bloodAdrenal Medulla in the venous circulation. When the cardiac muscle is stretched beforeThe fetal adrenal medulla produces epinephrine and norepinephrine contraction by an increased inflow of blood, it contracts with a greaterin response to stress. Both substances act on the heart and cardiovas- force and is able to pump out more blood. This mechanism of responsecular system in a way similar to sympathetic stimulation to produce a to preload is apparently not the same in the fetal heart as in the adultfaster FHR, greater force of contraction of the heart, and higher arterial heart. In the fetus, increases in preload produce minor, if any, changesblood pressure. in combined ventricular output, suggesting that the fetal heart nor- mally operates near the peak of its function curve.Renin-Angiotensin System The output of the fetal heart is essentially related to the FHR.Angiotensin II may play a role in fetal circulatory regulation at rest, Some researchers have shown that spontaneous variations of FHRbut its main activity is observed during hemorrhagic stress on a relate directly to cardiac output (i.e., as the rate increases, output alsofetus. increases). However, different responses have been observed during right or left atrial pacing studies.8 Clearly, additional factors areProstaglandins required to explain such differences. In addition to FHR and preload,Various prostaglandins and arachidonic acid metabolites are found in cardiac output depends on afterload and intrinsic contractility.8,9the fetal circulation and in many fetal tissues. Their main roles with The fetal heart appears to be highly sensitive to changes in afterload,respect to cardiovascular function seem to be regulating umbilical represented by the fetal arterial blood pressure. Increases in afterloadblood flow and maintaining the patency of the ductus arteriosus dramatically reduce the stroke volume or cardiac output. As alreadyduring fetal life. stated, the fetal heart is incompletely developed. Many ultrastructural differences between the fetal and adult heart account for a lower intrin-Other Hormones sic capacity of the fetal heart to alter its contraction efficiency. TheOther hormones, such as nitric oxide, α-melanocyte–stimulating determinants of cardiac output do not work separately; each interactshormone, atrial natriuretic hormone, neuropeptide Y, thyrotropin- dynamically to modulate the fetal cardiac output during changingreleasing hormone, cortisol, and metabolites such as adenosine, are physiologic conditions. In clinical practice, it is reasonable to assumealso present in the fetus and participate in the regulation of circulatory that modest variations of FHR from the normal range produce rela-function. tively small effects on the cardiac output. However, at the extremes
  3. 3. CHAPTER 22 Intrapartum Fetal Surveillance 399(e.g., tachycardia >240 beats/min, bradycardia <60 beats/min), cardiac Although this device is simple to apply, it is often inconsistent inoutput and umbilical blood flow are likely to be substantially decreased. obtaining a signal because of interference caused by maternal and fetal movements. Improvements in the logic and technology of the moni- tors have made the external devices more accurate and easier to use.Umbilical Blood Flow In particular, the technique of “autocorrelation” is now used to define the timing of the cardiac contraction more accurately. A very largeThe umbilical blood flow is approximately 40% of the combined fetal number of points on the “curve” depicting the Doppler frequency shiftventricular output, and not all of this blood flow to the placenta are analyzed, and this produces a signal that much more accuratelyexchanges with maternal blood. Umbilical blood flow is unaffected by represents the FHR variability.acute moderate hypoxia but is decreased by severe hypoxia affectingthe myocardial function. There is no innervation of the umbilical cord,and there are no known means of increasing umbilical flow. How- Uterine Activity Detectionever, variable decelerations in the FHR commonly occur withtransient umbilical cord compression, and flow is certainly diminished Intra-amniotic Catheteror stopped for a time, depending on the degree and duration of cord The internal means of detecting uterine activity typically uses a softcompression or occlusion. plastic, transducer-tipped catheter placed transcervically into the amniotic cavity. The pressure of the baseline uterine tone and that of any uterine contraction is translated into an electrical signal, whichFetal Heart Rate Monitor is calibrated and displayed directly (in millimeters of mercury of pressure).The electronic FHR monitor is a device with two components: Oneestablishes the FHR, and the other measures uterine contractions.10 To Tocodynamometerrecognize FHR, the device uses either the R wave of the fetal electro- The tocodynamometer is an external device that is placed on thecardiogram (ECG) complex (fetal scalp electrode) or the modulation maternal abdominal wall, over the uterine fundus. The tightening ofof an ultrasound signal generated by movement of a cardiovascular the fundus with each contraction is detected by pressure on a smallstructure (Doppler ultrasound transducer or cardiotachometer). button in the center of the transducer, and uterine activity is displayedUterine contractions are detected either directly, by a pressure trans- on the recorder. It acts just like a hand placed on the uterine fundusducer attached to a catheter within the amniotic cavity (intrauterine through the abdominal wall to detect uterine activity. This devicepressure catheter), or by an belt-like external device (tocodynamome- detects the frequency and duration of uterine contractions but not trueter) that recognizes the tightening of the uterus during a contraction. contraction intensity. One disadvantage of the tocodynamometer isMonitoring with devices attached directly to the fetus or placed within that it works best with the mother in the supine position. This limita-the uterine cavity is called “internal,” and monitoring with devices that tion may not always be compatible with maternal comfort, fetal well-are on the maternal abdomen is called “external.” being, or progression of labor. With repositioning of the patient, it is important to reestablish accurate monitoring of both the fetal heart and uterine activity.Fetal Heart Rate DetectionFetal ElectrodeThe fetal electrode consists of a small, stainless steel, spiral wire that is Fetal Responses totypically attached to the fetal scalp. A second contact is bathed by thevaginal fluids. The wires traverse the vaginal canal and are connected Hypoxia/Acidemiato a maternal leg plate, which in turn is attached to the fetal monitor. Studies of chronically prepared animals have shown that a number ofThe internal mode gives the most accurate FHR tracing, because this responses occur during acute hypoxia or acidemia in the previouslytechnique directly measures the fetal cardiac electrical signal and true normoxemic fetus. Little or no change in combined cardiac output andbeat-to-beat variability. umbilical (placental) blood flow occurs, but there is a redistribution of blood flow favoring certain vital organs—namely, heart, brain, andDoppler Ultrasound Transducer adrenal gland—and a decrease in blood flow to the gut, spleen, kidneys,The FHR monitoring device most commonly employed is the cardio- and carcass.11 This initial response is presumed to be advantageous totachometer or Doppler ultrasound transducer. This device emits a a fetus in the same way as the diving reflex is advantageous to an adulthigh-frequency ultrasound signal (approximately 2.5 MHz) that is seal, in that the blood containing the available oxygen and other nutri-reflected from any moving structure (e.g., ventricle wall, valvular leaf- ents is supplied preferentially to vital organs. This series of responseslets), with the reflected signal being altered in frequency. The change may be thought of as temporary compensatory mechanisms thatin frequency with each systole is recognized as a cardiac contraction enable a fetus to survive for moderately long periods (e.g., up to 30and is processed by the transducer. The interval between cardiac events minutes) of limited oxygen supply without decompensation of vitalis measured (in seconds) and then divided into 60 to yield a rate for organs, particularly the brain and heart.each interval between beats. These calculated rates are transcribed onto The close matching of blood flow to oxygen availability to achievea paper strip that is moving at a specific speed (usually 3 cm/min). The a constancy of oxygen consumption has been demonstrated in the fetalresulting tracing appears as a jiggly line and is a very close representa- cerebral circulation12 and in the fetal myocardium.13 In studies ontion of true FHR variability. If the intervals between heartbeats are hypoxic lamb fetuses, cerebral oxygen consumption was constant overpersistently identical, the resultant FHR line is straight, suggesting a wide range of arterial oxygen concentrations, because the decreaseminimal or absent variability. in arteriovenous oxygen content accompanying hypoxia was offset by
  4. 4. 400 CHAPTER 22 Intrapartum Fetal Surveillancean increase in cerebral blood flow. However, during more severe aci- placenta, where they diffuse slowly (in contradistinction to carbondemia or sustained hypoxemia, these responses were no longer main- dioxide) into the maternal circulation. The maternal kidney excretestained, and decreases in cardiac output, arterial blood pressure, and noncarbonic acids produced by both maternal and fetal metabolismblood flow to the brain and heart resulted.14 These changes may be and thus helps regenerate bicarbonate. Because the maternal glomeru-considered to be a stage of decompensation after which tissue damage lar filtration rate increases significantly during normal pregnancy, theand even fetal death may follow.15 The implications of such a scenario maternal kidney filters and reabsorbs large quantities of bicarbonateare of obvious importance to the fetus in utero. daily. The fetus does have the ability to metabolize accumulated lactate in the presence of sufficient oxygen; however, this is a slow process, and for practical purposes it is not thought to account for a large propor-Fetal Acid-Base Balance tion of lactic acid elimination from the fetal compartment.Physiology BuffersNormal metabolism in the fetus results in the production of both car- Dramatic changes in pH are minimized by the action of buffers. Thebonic and organic acids. These acids are buffered by various mecha- two major buffers are plasma bicarbonate and hemoglobin. Other,nisms which regulate the fetal pH within a very narrow range. Although quantitatively less important buffers include erythrocyte bicarbonatethe concentration of hydrogen ions is extremely low, changes in fetal and inorganic phosphates.19pH as small as 0.1 unit can have profound effects on metabolic activity Terms that are used for the expression of buffering capacity includeand on the cardiovascular and central nervous systems. Extreme the following:changes in pH can be fatal. The maternal acid-base status can adversely affect fetal acid-base 1. Delta base—a measure of “change” in the buffering capacity ofstatus. In normal pregnancies, the difference between maternal and bicarbonatefetal pH is usually 0.05 to 0.10 units.16 2. Base deficit—bicarbonate values lower than normal 3. Base excess—bicarbonate values higher than normalCarbonic AcidCarbonic acid (H2CO3) is a volatile acid that is produced from the Although the fetus has a limited ability to buffer an increase in acidmetabolism of glucose and fatty acids. During fetal oxidative metabo- production with bicarbonate and hemoglobin, the placental bicarbon-lism (i.e., aerobic glycolysis or cellular respiration), the oxidation of ate pool could also play a role in buffering the fetus against changes inglucose uses oxygen (O2) and produces carbon dioxide (CO2). maternal pH or blood gas status. Aarnoudse and colleagues20 studied From a practical standpoint, carbonic acid formation is equivalent bicarbonate permeability in the perfused human placental cotyledonto carbon dioxide generation, and most of the free hydrogen ion model and found that acidification of the maternal circulation to pHformed is buffered intracellularly. As blood passes through the placenta 7.06 for 30 minutes did not significantly alter fetal pH. Instead, there(or through the lung in the adult), bicarbonate ion (HCO3−) reenters was an efflux of total carbon dioxide from the placenta into the mater-erythrocytes and combines with hydrogen ions to form carbonic acid, nal circulation in the form of bicarbonate, which was not matched bywhich then dissociates to carbon dioxide and water. The carbon dioxide an influx of total carbon dioxide from the fetal circulation. By thisthus formed in the fetus diffuses across the placenta and is excreted by mechanism, bicarbonate transfer could take place between the placen-the maternal lung. Carbon dioxide diffuses rapidly across the human tal tissue pool and the maternal circulation, while the transmission ofplacenta, so that even large quantities produced by the fetus can be maternal pH and blood gas changes to the fetal circulation would beeliminated rapidly if maternal respiration, uteroplacental blood flow, minimized.and umbilical blood flow are normal. The rate of fetal carbon dioxide production is roughly equivalent pH Determinationto the fetal oxygen consumption rate.17 In order for carbon dioxide to The pH is a measure of the acid-base status of various body fluids.diffuse from fetus to mother, a gradient must be maintained between Specifically, pH is the negative logarithm of the hydrogen ion con-PCO2 in fetal umbilical blood and that in maternal uteroplacental centration. It is directly related to the concentration of bicarbonateblood; in addition, adequate perfusion of both sides of the placenta (base) and inversely related to the concentration of carbonic acidmust be preserved. Secondary to progesterone-stimulated maternal (acid). The H2CO3 equals 0.03 × PCO2 and the pK equals 6.11hyperventilation, the maternal arterial PCO2 is reduced from a mean for normal plasma at 37°C. This relation is best illustrated by theof 39 mm Hg during nonpregnancy to a mean of 31 mm Hg during Henderson-Hasselbalch equation for determining the pH of a bufferedpregnancy. Renal compensation, in turn, results in an increase in bicar- system, in which pK is the negative logarithm of the acid dissociationbonate excretion, resulting in plasma levels of 18 to 22 mEq/L during constant:pregnancy.18 [ base] pH = pK + logNoncarbonic Acids [acid ]Anaerobic metabolism in the fetus results in the production of non-volatile or noncarbonic acids via two mechanisms: (1) use of non– In the case of fetal acid-base balance determinations,sulfur-containing amino acids, which results in uric acid formation,and (2) incomplete combustion of carbohydrates and fatty acids, pH = pK + log [HCO3− ]which results in the production of lactic acid and the ketoacids (e.g., [H2CO3 ]β-hydroxybutyric acid). Because of relatively immature renal function, the fetus is unable pH = pK + log [HCO3− ](mEq/L )to effectively excrete these acids; instead, they are transported to the 0.03[PCO2 ](mm Hg )
  5. 5. CHAPTER 22 Intrapartum Fetal Surveillance 401 In simplest terms, the HCO3− represents the “metabolic” com- Removal of carbon dioxide depends on fetal blood flow to theponent, whereas the H2CO3 (or PCO2) represents the “respiratory” placenta and transport across the placenta. Fixed-acid equilibriumcomponent.21 depends on a continued state of balance between production and removal.Terminology Respiratory FactorsAcidemia refers to an increase in hydrogen ions in the blood; acidosis Respiratory acidosis results from increased PCO2 and subsequentlyrefers to an increase in hydrogen ions in tissue. Similarly, hypoxemia is decreased pH. In the fetus, this picture is usually associated with aa decrease in oxygen content in blood, whereas hypoxia is a decrease decrease in PO2 as well. The most common cause of acute respiratoryin oxygen content in tissue (Table 22-1). acidosis in the fetus is a sudden decrease in placental or umbilical Although an umbilical artery pH of less than 7.20 has traditionally perfusion. Umbilical cord compression, uterine hyperstimulation, andbeen used to define newborn acidemia, most clinicians define acidemia abruptio placentae are good examples, with transient cord compres-as two standard deviations below the mean umbilical artery pH (7.10 sion being the most common factor.to 7.18). The concept of clinically significant or “pathologic” acidemia Conditions associated with maternal hypoventilation or hypoxiais discussed later in this chapter. can also result in respiratory acidosis in the fetus (and in metabolic Acidemia in the newborn can be classified into three basic types: acidosis, if severe enough). Coleman and Rund23 reviewed themetabolic, respiratory, and mixed. The type is based primarily on the association of maternal hypoxia with nonobstetric conditions (e.g.,levels of HCO3− and PCO2 (Table 22-2). With marked elevations of the asthma, epilepsy) during pregnancy, noting that the normal physio-PCO2, there is a compensatory increase in HCO3− of 1 mEq/L for each logic changes that occur during pregnancy may make early recognition10 mm Hg increase in PCO2.22 of maternal hypoxia difficult. For example, in a mother with asthma, a pH of less than 7.35 and a PCO2 higher than 38 mm Hg could indicate respiratory compromise.24 To minimize the risk of concurrent hypox-Factors Affecting Acid-Base Balance emia in the fetus, early intubation in mothers who have borderlineWith regard to acid-base balance in the fetus, the placenta acts as both or poor blood gas values or evidence of respiratory compromise is“lungs” and “kidneys” by supplying oxygen and removing carbon recommended.dioxide and various metabolites. The pH in the fetus is thus controlled Other conditions can result in maternal hypoventilation (acute orwithin a very tight range. Umbilical blood oxygen content and satura- chronic) during pregnancy. Induction of anesthesia or narcotic over-tion and fetal arterial delta base depend primarily on uterine blood dose can depress the medullary respiratory center. Hypokalemia, neu-flow. Oxygen supply, in turn, depends on the following: romuscular disorders (e.g., myasthenia gravis), and drugs that impair neuromuscular transmission (e.g., magnesium sulfate) can, in toxic Adequate maternal oxygenation doses, result in hypoventilation or even paralysis of the respiratory Blood flow to the placenta muscles. Finally, airway obstruction from foreign bodies can also result Transfer across the placenta in maternal respiratory acidosis. Restoration of normal fetal acid-base Fetal oxygenation balance depends on the reversibility of maternal etiologic factors. Delivery to fetal tissues Maternal respiratory alkalosis may occur when hyperventilation reduces the PCO2 and subsequently increases pH. Severe anxiety, acute salicylate toxicity, fever, sepsis, pneumonia, pulmonary emboli, and acclimation to high altitudes are etiologic factors. As in respiratory TABLE 22-1 TERMINOLOGY acidosis, restoration of the maternal acid-base balance by appropriate Acidemia Increased concentration of hydrogen ions in blood treatment of causative factors results in normalization of fetal blood Acidosis Increased concentration of hydrogen ions in tissue gases. Asphyxia Hypoxia with metabolic acidosis Base deficit HCO3− concentration lower than normal Metabolic Factors Base excess HCO3− concentration higher than normal Fetal metabolic acidosis is characterized by loss of bicarbonate, high Delta base Measure of change in buffering capacity of base deficit, and a subsequent fall in pH. This type of acidosis results bicarbonate from protracted periods of oxygen deficiency to a degree that results Hypoxemia Decreased oxygen content in blood Hypoxia Decreased level of oxygen in tissue in anaerobic metabolism. The etiology can be fetal or maternal and pH Negative logarithm of hydrogen ion concentration usually implies the existence of a chronic metabolic derangement. Conditions such as growth restriction resulting from chronic uteropla- Adapted from American College of Obstetricians and Gynecologists: cental hypoperfusion can be associated with fetal metabolic acidosis Umbilical Artery Blood Acid-Base Analysis. Technical Bulletin No. 216. secondary to decreased oxygen delivery. Washington, DC, ACOG, November 1995. Maternal metabolic acidosis can also cause fetal metabolic acidosis and is classified according to the status of the anion gap. In addition to bicarbonate and chloride, the remaining anions required to balance TABLE 22-2 TYPES OF ACIDEMIA* the plasma sodium concentration are referred to as “unmeasured anions” or the anion gap. Reduced excretion of inorganic acids (as Metabolic Normal PCO2 and decreased HCO3− in renal failure) or accumulation of organic acids (as in alcoholic, Respiratory Increased PCO2 and normal HCO3− (after correction diabetic, or starvation ketoacidosis and lactic acidosis) results in an of PCO2) Mixed Increased PCO2 and decreased HCO3− increased anion gap metabolic acidosis. Bicarbonate loss (as in renal tubular acidosis, hyperparathyroidism, and diarrheal states) or failure *Umbilical artery pH <7.10. of bicarbonate regeneration results in metabolic acidosis characterized
  6. 6. 402 CHAPTER 22 Intrapartum Fetal Surveillance TABLE 22-3 FETAL SCALP BLOOD VALUES IN LABOR* Measurement Early First Stage Late First Stage Second Stage pH 7.33 ± 0.03 7.32 ± 0.02 7.29 ± 0.04 PCO2 (mm Hg) 44.00 ± 4.05 42.00 ± 5.1 46.30 ± 4.2 PO2 (mm Hg) 21.8 ± 2.6 21.3 ± 2.1 16.5 ± 1.4 Bicarbonate (mMol/L) 20.1 ± 1.2 19.1 ± 2.1 17 ± 2 Base excess (mMol/L) 3.9 ± 1.9 4.1 ± 2.5 6.4 ± 1.8 *Mean ± standard deviation. From Huch R, Huch A: Maternal-fetal acid-base balance and blood gas measurement. In Beard RW, Nathanielsz PW (eds): Fetal Physiology and Medicine. New York, Marcel Dekker, 1984, p 713.by a normal anion gap. Fetal responses to these maternal conditions 10,000 U/mL of heparin to 0.2 mL of blood significantly decreased theare manifested by a pure metabolic acidosis with normal respiratory pH, PCO2, and bicarbonate. Therefore, any residual heparin (as well asgas exchange as long as placental perfusion remains normal. air) should be ejected, and the needle should be capped. Prolonged fetal respiratory acidosis (as in cord compression and A few practical points merit mention. First, it is not necessary toabruptio placentae) can also result in accumulation of noncarbonic draw the sample from the umbilical artery immediately, provided thatacids produced by anaerobic metabolism; this condition is character- the cord is clamped. Adequate specimens have been obtained from aized by blood gas measurements that reflect a mixed respiratory and clamped segment of cord as long as 60 minutes after delivery withoutmetabolic acidosis. significant changes in pH or PCO2.30 Moreover, once the specimens have been drawn into the syringe, they are relatively stable at roomEffects of Labor temperature for up to 60 minutes31 and do not need to be transportedEach uterine contraction transiently diminishes uterine blood flow, to the laboratory on ice.32 The same may not be true for specimensreduces placental perfusion, and impairs transplacental gaseous obtained from placental vessels.33exchange. A sample of blood may be obtained from the fetal presenting Chauhan and colleagues34 prepared a mathematical model thatpart to help evaluate fetal status during labor. Typical fetal scalp blood allows for the calculation of umbilical artery pH for up to 60 hoursvalues during labor are shown in Table 22-3. after delivery. This model permits the estimation of fetal pH at birth.Umbilical Cord Blood Normal Values Although there is no consensus as to what the most appropriate umbil-Acid-Base Analysis ical artery pH cutoff should be to define acidemia, the mean pH valuesUmbilical cord blood acid-base analysis provides an objective method from four studies are shown in Table 22-4. The mean value for umbili-of evaluating a newborn’s condition, especially with regard to hypoxia cal artery pH appears to be very close to 7.28. The subjects in the studyand acidemia.16 Assessing umbilical cord blood pH has become an reported by Riley and Johnson27 were from 3522 unselected womenimportant adjunct in defining perinatal hypoxia that is severe enough undergoing vaginal delivery.to result in acute neurologic injury.25 Moreover, the technique is simple The mean pH for umbilical venous blood has been reported to beand relatively inexpensive. 7.32 to 7.35. In a study of umbilical venous blood pH, D’Souza and associates28 reported a mean venous pH of 7.34 (± 0.07). Huisjes andTechnique Aarnoudse35 also reported good correlation between umbilical venousA segment of cord (approximately 10 to 20 cm) should be doubly and arterial pH.clamped immediately after delivery in all women, in the event that cord Although the Apgar scores of premature infants may be low becauseblood analysis is desired or deemed necessary. The cord is clamped of immaturity, mean values for both arterial and venous pH and bloodimmediately because a delay as short as 20 seconds can significantly gas values are similar to those of the term infant. Mean values foralter the arterial pH and PCO2.26 Specimens should be obtained ideally almost 2000 premature infants are summarized in Table 22-5.from the umbilical artery and the umbilical vein, but the umbilicalartery sample provides a more direct assessment of fetal condition, Pathologic Fetal Acidemiawhereas the umbilical vein reflects placental acid-base status. In cases What level of umbilical artery pH should be considered abnormal,such as cord prolapse, the umbilical artery pH may be extremely low, “pathologic,” or clinically significant? It is now well established that theeven in the presence of a normal umbilical vein pH.27 Nevertheless, former pH cutoff of 7.20 is not appropriate.16,36 Most newborns withsome clinicians still prefer to use the umbilical vein, which is easier to an umbilical artery pH lower than 7.20 are vigorous and without sys-access for drawing blood, especially in the very premature infant. In temic evidence of hypoxia. Recent evidence suggests that significantone study of 453 term infants, D’Souza and colleagues28 determined neonatal morbidity is more likely to occur in neonates with umbilicalthat umbilical venous and arterial blood pH are significantly related to artery pH values lower than 7.00, especially if associated with a loweach other and that umbilical venous pH measurements do provide Apgar score (i.e., ≤3). For example, in a study of 2738 term newborns,useful information regarding newborn acidemia at birth. hypotonia, seizures, and need for intubation were significantly corre- Samples should be drawn in plastic or glass syringes that have been lated with an umbilical artery pH of less than 7.00 and an Apgar scoreflushed with heparin (1000 U/mL). Commercial syringes (1 to 2 mL) of 3 or less at 1 minute.37 The authors concluded that a newborn mustcontaining lyophilized heparin are also available for obtaining speci- be severely depressed at birth for birth hypoxia to be implicated as themens. Kirshon and Moise29 reported that the addition of 0.2 mL of cause of seizures.
  7. 7. CHAPTER 22 Intrapartum Fetal Surveillance 403 TABLE 22-4 NORMAL UMBILICAL CORD BLOOD pH AND BLOOD GAS VALUES IN TERM NEWBORNS (MEAN ± SD) Yeomans et al., 1985 Ramin et al., 1989 Riley and Johnson, 1993 Thorp et al., 1989 Measurement (n = 146) (n = 1292) (n = 3520) (n = 1924) Arterial Blood (n = 1694) pH 7.28 ± 0.05 7.28 ± 0.07 7.27 ± 0.07 7.24 ± 0.07 PCO2 (mm Hg) 49.20 ± 8.4 49.90 ± 14.2 50.30 ± 11.1 56.30 ± 8.6 HCO3− (mEq/L) 22.30 ± 2.5 23.10 ± 2.8 22.00 ± 3.6 24.10 ± 2.2 Base excess (mEq/L) — −3.60 ± 2.8 −2.70 ± 2.8 −3.60 ± 2.7 Venous Blood (n = 1820) pH 7.35 ± 0.05 — 7.34 ± 0.06 7.32 ± 0.06 PCO2 (mm Hg) 38.20 ± 5.6 — 40.70 ± 7.9 43.80 ± 6.7 HCO3− (mEq/L) 20.40 ± 4.1 — 21.40 ± 2.5 22.60 ± 2.1 Base excess (mEq/L) — — −2.40 ± 2.0 2.90 ± 2.4 Data from Yeomans ER, Hauth JC, Gilstrap LC, et al: Umbilical cord pH, PCO2 and bicarbonate following uncomplicated term vaginal deliveries. Am J Obstet Gynecol 151:798, 1985; Ramin SM, Gilstrap LC, Leveno KJ, et al: Umbilical artery acid-base status in the preterm infant. Obstet Gynecol 74:256, 1989; Riley RJ, Johnson JWC: Collecting and analyzing cord blood gases. Clin Obstet Gynecol 36:13, 1993; Thorp JA, Boylan PC, Parisi VM, et al: Effects of high-dose oxytocin augmentation on umbilical cord blood gas values in primigravid women. Am J Obstet Gynecol 159:670, 1988. TABLE 22-5 NORMAL ARTERY BLOOD GAS TABLE 22-6 NEONATAL MORBIDITY AND VALUES FOR PREMATURE INFANTS MORTALITY ACCORDING TO (MEAN ± SD) pH CUTOFF Dickenson et al., Riley and Johnson, Measurement 1992 (n = 949) 1993 (n = 1015) pH 7.27 ± 0.07 7.28 ± 0.089 PCO2 (mm Hg) 51.60 ± 9.4 50.20 ± 12.3 HCO3− (mEq/L) 23.90 ± 2.1 22.40 ± 3.5 Base excess (mEq/L) −3.00 ± 2.5 −2.50 ± 3.0 From Dickenson JE, Eriksen NL, Meyer BA, et al: The effect of preterm birth on umbilical cord blood gases. Obstet Gynecol 79:575, 1992; Riley From Goldaber KG, Gilstrap LC, Leveno KJ, et al: Pathologic fetal RJ, Johnson JWC: Collecting and analyzing cord blood gases. Clin acidemia. Obstet Gynecol 78:1103, 1991. Obstet Gynecol 36:13, 1993. Goldaber and coworkers,22 in an attempt to better define the critical those without this diagnosis (6.93; 25th to 75th percentile, 6.85 to 6.97;cutoff for pathologic fetal acidemia, studied the neonatal outcome of P = .03). The median pH was also less than 6.90 in newborns who3506 term newborns. They determined the critical pH cutoff point to required intubation (6.83) or cardiopulmonary resuscitation (6.83)be 7.00 (Table 22-6). Many of these babies, however, had no complica- and was significantly lower (P < .05) than in newborns without thesetions and went to the newborn nursery. In a follow-up study from the complications It should also be noted that the median PCO2 and basesame institution, King and associates38 reported on 35 term newborns deficit were significantly higher in neonates with these morbidities.40with an umbilical artery pH greater than 7.00 who were triaged to thenewborn nursery. These authors concluded that term newborns who Acute Neurologic Injuryhad this degree of acidemia at birth but had a stable appearance in the There is poor correlation between neurologic outcome and thedelivery room (and were without other complications) did not have 1-minute and 5-minute Apgar scores. The correlation does improve ifevidence of hypoxia or ischemia during the 48 hours after birth. It has the scores remain between 0 and 3 at 10, 15, and 20 minutes; however,been reported that fewer than half of neonates with an umbilical artery many such babies will still be “normal” if they survive. Similarly, a lowpH lower than 7.00 actually have neonatal complications.39 umbilical artery pH in and of itself also has poor correlation with The critical pH cutoff for neonatal morbidity may actually be even adverse outcome. The American College of Obstetricians and Gyne-lower than 7.00. Data presented by Andres and colleagues40 suggest a cologists (ACOG)41 has established the following essential criteria (allvalue closer to 6.90. In a review of 93 neonates (>34 weeks’ gestational four must be met) to indicate hypoxia proximate to delivery severeage) with an umbilical artery pH greater than 7.00, the median pH for enough to be associated with acute neurologic injury:the group was 6.92 (range, 6.62 to 6.99); however, the median pH was6.75 for neonates with seizures (25th to 75th percentile, 6.72 to 6.88), 1. Evidence of a metabolic acidosis in fetal umbilical cord arterialcompared with 6.93 for those without seizures (P = .02). The median blood obtained at delivery (pH <7 and base deficit ≥12 mmol/L)pH for newborns with hypoxic-ischemic encephalopathy was also sig- 2. Early onset of severe or moderate neonatal encephalopathy innificantly lower (6.69; 25th to 75th percentile, 6.62 to 6.75) than for infants born at 34 or more weeks of gestation
  8. 8. 404 CHAPTER 22 Intrapartum Fetal Surveillance3. Cerebral palsy of the spastic quadriplegic or dyskinetic type versus 0%; P < .05). These authors, however, used an umbilical artery4. Exclusion of other identifiable etiologies, such as trauma, coagula- pH cutoff of 7.25 to define acidemia. tion disorders, infectious conditions, or genetic disorders In another report of 323 newborns with meconium by Yeomans and associates,49 there was a significantly increased frequency of meco- In two publications, Low and associates42,43 reported on the associa- nium below the cords in acidemic fetuses than in nonacidemic fetusestion of severe or significant metabolic acidosis (as determined by the (31% versus 18%; P < .05). Meconium aspiration syndrome, however,umbilical artery blood gas profile) and newborn complications. Low43 was an uncommon event, occurring in only 3% of newborns. Raminproposed a classification of intrapartum fetal asphyxia, the severity of and colleagues,50 in a study of meconium, reported that 55% of meco-which is based on newborn encephalopathy and other organ system nium aspiration syndrome cases occurred in newborns with an umbili-dysfunction. cal artery pH greater than 7.20. In a review of 4985 term neonates born to mothers with meco-Other Clinical Events and Umbilical Blood nium-stained amniotic fluid, Blackwell and colleagues51 identified 48Acid-Base Analysis cases of severe meconium aspiration syndrome in which umbilical artery pH measurements were obtained; the pH was 7.20 or higher inBeyond its use in assessing prematurity and neurologic injury, um- 29 of these patients and less than 7.20 in 19. There was no differencebilical blood gas analysis has been reported in a variety of clinical in frequency of seizures between the two pH groups. The authorssituations, such as acute chorioamnionitis, nuchal cords, meconium, concluded that severe meconium aspiration syndrome occurred in theprolonged pregnancy, FHR anomalies, operative vaginal delivery, presence of normal acid-base status at delivery in many of the cases,breech delivery, and use of oxytocin.36 Such analysis may also prove suggesting that a “preexisting injury or a nonhypoxic mechanism isuseful in assessing the interval to delivery in shoulder dystocia cases. often involved.”51 ACUTE CHORIOAMNIONITIS PROLONGED PREGNANCY In one study of 123 women with acute chorioamnionitis, compared In a study of 108 women with a prolonged pregnancy, Silver andwith more than 6000 noninfected women, Maberry and coauthors44 colleagues52 reported a mean umbilical artery pH of 7.25. Moreover,found no significant association between infection and fetal acidemia significantly more newborns who were delivered for FHR indications(Table 22-7). Hankins and colleagues45 found no association between had acidemia than newborns who were not (45% versus 13%;acute chorioamnionitis and newborn acidemia. Meyer and colleagues,46 P < .05).however, reported an association of fetal sepsis with a decrease inumbilical artery pH compared with controls (7.21 versus 7.26). FETAL HEART RATE ABNORMALITIES Gilstrap and colleagues,53 in a study of 403 term newborns with NUCHAL CORDS FHR abnormalities in the second stage of labor compared with 430 In a study of 110 newborns with nuchal cords, Hankins and col- control newborns, reported an association of abnormalities and acide-leagues47 reported that significantly more newborns with nuchal cords mia (Table 22-8). This was confirmed in a follow-up study.54 Honjowere acidemic (umbilical artery pH <7.20), compared with controls and Yamaguchi55 also reported a correlation between second-stage(20% versus 12%; P < .05); however, there were no significant differ- baseline FHR abnormalities and fetal acidemia at birth. Although thereences in mean pH (7.25 versus 7.27); PCO2 (49 versus 48 mm Hg), or may be an association between FHR abnormalities and acidemia, theHCO3− (20.5 versus 21.0 mEq/L). association with adverse long-term neurologic outcome is uncommon. For example, Nelson and colleagues,56 in a population-based study of MECONIUM children with cerebral palsy and a birth weight of 2500 g or more, In one study of 53 term pregnancies with moderate to thick meco- reported that specific FHR abnormalities (i.e., late deceleration andnium, Mitchell and colleagues48 reported that approximately half of the decreased beat-to-beat variability) were associated with an increasednewborns were acidemic, and that significantly more acidemic new- risk of cerebral palsy. However, of all the children with these abnormalborns had meconium below the cords, compared with controls (32% FHR findings only 0.19% had cerebral palsy. Therefore, the false-posi- tive rate was 99.8%. TABLE 22-7 COMPARISON OF UMBILICAL ARTERY pH IN PATIENTS WITH TABLE 22-8 ASSOCIATION OF UMBILICAL AND WITHOUT ACUTE ARTERY ACIDEMIA AND SECOND- CHORIOAMNIONITIS STAGE FETAL HEART RATE (FHR) ABNORMALITIES IN NEWBORNS Patients with Chorioamnionitis Controls FHR Pattern N Umbilical Artery pH <7.20 Umbilical Artery pH (n = 123) (n = 6769) Tachycardia* 117 15% <7.20 18 (15.0%) 701 (10.0%) Mild bradycardia* 165 18% <7.15 4 (3.0%) 242 (4.0%) Moderate/marked bradycardia* 121 27% <7.00 0 6 (0.1%) Normal 430 4% Metabolic acidemia 1 (0.8%) 9 (0.1%) *P < .0001 compared with normals. From Maberry MC, Ramin SM, Gilstrap LC, et al: Intrapartum asphyxia Modified from Gilstrap LC, Hauth JC, Toussaint S: Second stage fetal in pregnancies complicated by intraamniotic infection. Obstet Gynecol heart rate abnormalities and neonatal acidosis. Obstet Gynecol 63:209, 76:351, 1990. Reprinted with permission from the American College of 1984. Reprinted with permission from the American College of Obstetricians and Gynecologists. Obstetricians and Gynecologists.
  9. 9. CHAPTER 22 Intrapartum Fetal Surveillance 405 TABLE 22-9 METHOD OF DELIVERY AND cord blood measurements for all cesarean deliveries and instrumental FETAL ACIDEMIA deliveries for fetal distress. The ACOG41 recommends umbilical cord blood acid-base analysis in the following situations: Method of Delivery N % with Acidemia* Cesarean delivery for fetal compromise Spontaneous 303 7 Low 5-minute Apgar score Elective outlet/low forceps 177 9 Indicated outlet/low forceps 293 18 Severe growth restriction Indicated midforceps 234 21 Abnormal FHR tracing Cesarean delivery 111 18 Maternal thyroid disease Intrapartum fever *Umbilical artery pH <7.20. Multifetal gestations From Gilstrap LC, Hauth JC, Shiano S, et al: Neonatal acidosis and method of delivery. Obstet Gynecol 63:681, 1984. Reprinted with permission from the American College of Obstetricians and Gynecologists. Characteristics of Fetal OPERATIVE VAGINAL DELIVERY Heart Rate Patterns Gilstrap and coworkers57 found no significant difference in the fre-quency of newborn acidemia according to method of delivery (Table Basic Patterns22-9). This was true even when the indication for delivery was fetal The characteristics of the FHR pattern are classified as baseline ordistress. periodic/episodic.65,66 The baseline features—rate and variability—are those recorded between uterine contractions. Periodic changes occur BREECH DELIVERY in association with uterine contractions, and episodic changes are those Although the mean umbilical artery pH was lower for infants deliv- not obviously associated with uterine contractions.ered vaginally in breech presentations compared with cephalic presen-tations in two studies,58,59 pH levels were not significantly low from a Baseline Featuresclinical standpoint (7.23 and 7.16, respectively). It seems unlikely that The baseline features of the FHR are those predominant characteristicsdelivery of breech presentations by the vaginal route is related to sig- that can be recognized between uterine contractions. They are thenificant newborn acidemia. baseline rate and variability of the FHR. SHOULDER DYSTOCIA BASELINE RATE Most adverse outcomes associated with shoulder dystocia are due The definition of baseline rate is the FHR recorded between con-to actual physical injury to the brachial plexus60 and not to acidemia tractions. More rigidly described, it is the approximate mean FHRor asphyxia (unless an extremely protracted period is needed to extract rounded to 5 beats/min during a 10-minute segment, excluding thethe fetus). In a review of 134 infants born after shoulder dystocia, following: (1) periodic or episodic changes, (2) periods of marked FHRStallings and colleagues61 reported that this complication was associ- variability, and (3) segments of the baseline that differ by at least 25ated with a “statistically significant but clinically insignificant” reduc- beats/min. In any 10-minute window, the minimum baseline durationtion in mean umbilical artery pH levels, compared to their obstetric must be at least 2 minutes; otherwise, the baseline for that period ispopulation (7.23 versus 7.27). indeterminate. The normal baseline FHR is between 110 and 160 beats/min. Rates OXYTOCIN slower than 110 beats/min are termed bradycardia, and rates faster than In a study of 556 women who received oxytocin compared with 160 beats/min are termed tachycardia. Baseline bradycardia and tachy-704 who did not, Thorp and colleagues62 found no significant dif- cardia are quantified by the actual rate observed in keeping with theference in mean umbilical artery pH measurements (7.23 versus 7.24, definition of baseline rate.respectively). FETAL HEART RATE VARIABILITY Electronic fetal heart rate monitoring (EFM) in most cases pro-Summary duces a tracing with an irregular line, demonstrating the FHRThe fetus maintains its pH within a very limited range and is depen- variability. The irregularities represent the slight differences in timedent on the placenta and the maternal circulation to maintain acid- interval, and therefore in calculated FHR, that occur from beat to beat.base balance. Several methods for assessing fetal-newborn acid-base If all intervals between heartbeats were identical, the line would bestatus have been described. Of these methods, umbilical blood gas straight. Fluctuations in the baseline FHR are irregular in amplitudeanalysis is probably the most useful and the easiest (and relatively the and frequency. (A pattern called “sinusoidal,” discussed later, differsleast expensive) to perform. from variability in that it has a smooth sine wave of regular frequency There are few data to justify a policy of umbilical blood gas analysis and amplitude and therefore is excluded from the definition of FHRfor all newborns. In a survey of 133 universities in the United States, variability.)Johnson and Riley63 reported that approximately 27% of centers used Baseline variability is defined as fluctuations in the FHR of 2 orcord blood for assessing newborn acid-base status in all deliveries. more cycles per minute and is quantitated as the peak-to-troughTwo thirds of the programs used them for tracing abnormal FHRs amplitude of the FHR in beats per minute. Variability is absent whenor for low Apgar scores. The Royal College of Obstetricians and the amplitude range is undetectable. It is minimal when there is anGynecologists and the Royal College of Midwives64 recommend routine amplitude range but it is less than 5 beats/min. Variability is normal or
  10. 10. 406 CHAPTER 22 Intrapartum Fetal Surveillancemoderate when the amplitude is between 6 and 25 beats/min. Vari- and seconds from the beginning to the end of the deceleration. Accel-ability is marked when the amplitude ranges greater than 25 beats/ eration is quantified similarly. Decelerations are defined as recurrentmin67 (see Classification and Significance of Baseline Variability). or persistent if they occur with more than 50% of uterine contractions in any 20-minute period. Bradycardia and tachycardia are quantifiedPeriodic Heart Rate Patterns by the actual FHR in beats per minute.Periodic patterns are the alterations in FHR that are associated withuterine contractions or changes in blood flow within the umbilicalcord vessels. These patterns are termed late decelerations, early decel- Normal and Abnormal Hearterations, variable decelerations, and accelerations. In each case, the Rate Patternsdecrease or increase in FHR is calculated from the most recently deter- The normal or reassuring FHR pattern (Fig. 22-1) is accepted asmined portion of the baseline. that with a baseline FHR of between 110 and 160 beats/min; an FHR variability amplitude between 6 and 25 beats/min; and no decelerative LATE DECELERATIONS periodic changes (although there may be periodic or episodic accelera- In late deceleration of the FHR, there is a visually apparent decrease tions). It is widely accepted in clinical practice that a fetus born withand subsequent return to baseline FHR that is associated with a uterine this FHR pattern is normally oxygenated if delivery occurs when thecontraction. The decrease is gradual, with the time from onset of normal FHR pattern is traced.4,68,69deceleration to nadir being at least 30 seconds, and is delayed in timing, In contrast to the high predictability of fetal normoxia and vigorwith the nadir of the deceleration occurring late in relation to the peak in the presence of the normal pattern, variant patterns are not asof the uterine contraction. In most cases, the onset, nadir, and recovery accurately predictive of fetal compromise. However, when these non-are all late in relation to the beginning, peak, and ending of the con- reassuring patterns are placed in the context of the clinical case (e.g.,traction, respectively. the progressive change in the patterns, the duration of the variant pat- terns), one can make reasonable judgments about the likelihood of EARLY DECELERATIONS fetal decompensation. With this screening approach, impending intol- Early deceleration of the FHR is similar to late deceleration erable fetal acidosis can be presumed or, in certain cases, ruled out byexcept that the decrease is coincident in timing, with the nadir of the the use of ancillary techniques (e.g., fetal scalp stimulation, vibro-deceleration occurring at the same time as the peak of the uterine acoustic stimulation, fetal scalp blood sampling).contraction. In most cases, the onset, nadir, and recovery are all coin- As a predictor for significant neurologic morbidity such as cerebralcident with the beginning, peak, and ending of the contraction, palsy, EFM has a very poor specificity and positive predictive value.respectively. The positive predictive value of a nonreassuring FHR is stated to be 0.14%. This means that for every 1000 fetuses born with a nonreassur- VARIABLE DECELERATIONS ing FHR tracing, 1 or 2 of them develop cerebral palsy.70 Thus, the Variable deceleration is defined as a visually apparent abrupt false-positive rate is greater than 99%.decrease (less than 30 seconds from onset of deceleration to beginningof nadir) in FHR from the baseline. The decrease in FHR is at least 15 Baseline Ratebeats/min, and its duration (from baseline to baseline) is at least 15 BRADYCARDIAseconds but not more than 2 minutes. When variable decelerations are Bradycardia is defined as a baseline FHR slower than 110 beats/min.associated with uterine contractions, their onset, depth, and duration Certain fetuses have a baseline FHR of less than 110 beats/min and arecommonly vary with successive contractions. cardiovascularly normal. Their baseline FHR simply represents a varia- Prolonged deceleration is a visually apparent abrupt decrease in FHR tion outside the limits of normal. Others with an FHR slower than 110below the baseline of at least 15 beats/min that has a duration between beats/min may have congenital heart block and a well-compensated2 and 10 minutes from onset to return to baseline. status despite a low FHR. Bradycardia is a term that relates to baseline FHR and is distin- ACCELERATIONS guished from a deceleration. However, a prolonged deceleration result- Acceleration is defined as a visually apparent abrupt increase (<30 ing in a new baseline bradycardia may result from vagal activity inseconds from onset of acceleration to peak) in FHR above the baseline. response to fetal hypoxia (Fig. 22-2). Reasons for such decreases inThe acme is at least 15 beats/min above the baseline, and the accelera- FHR include the following:tion lasts between 15 seconds and 2 minutes from onset to return tobaseline. Before 32 weeks of gestation, accelerations are defined as 1. A sudden drop in oxygenation, such as occurs with placental abrup-having an acme of at least 10 beats/min above the baseline and a dura- tion, maternal apnea, or amniotic fluid embolustion of at least 10 seconds. Prolonged acceleration is an acceleration 2. A decrease or cessation in umbilical blood flow, such as occurs withthat lasts at least 2 minutes but less than 10 minutes. a prolapsed cord or uterine rupture There is a close association between the presence of accelerations 3. A decrease in uterine blood flow, such as occurs with severe mater-and normal FHR variability. At times it may be difficult to decide nal hypotensionwhether a recorded pattern represents “acceleration” or a normal long-term variability complex. The final decision is not important, because TACHYCARDIAboth accelerations and normal variability have the same positive prog- Tachycardia is defined as a baseline FHR of more than 160 beats/nostic significance, indicating normal fetal oxygenation. min; it is distinguished from an acceleration in that its duration is at least 10 minutes. With tachycardia, there is commonly a loss of vari- QUANTIFICATION ability of the FHR. Although fetal tachycardia is potentially associated Any deceleration is quantified by the depth of the nadir in beats with fetal hypoxia, particularly when it is accompanied by decelera-per minute below the baseline. The duration is quantified in minutes tions of the FHR, the more common association is with maternal or
  11. 11. CHAPTER 22 Intrapartum Fetal Surveillance 407 FIGURE 22-1 Normal fetal heart rate pattern. The tracing exhibits normal rate (approximately 130 beats/ min), normal variability (amplitude range about 15 beats/min), and absence of periodic changes. This pattern represents a nonacidemic fetus without evidence of hypoxic stress. Uterine contractions are 2 to 3 minutes apart and about 60 to 70 mm Hg in intensity. FIGURE 22-2 Prolonged fetal bradycardia resulting from excessive oxytocin-induced hyperstimulation of the uterus after intravenous infusion of meperidine (Demerol) and promethazine (Phenergan) into the same tubing. The heart rate is returning to normal at the end of the tracing, after appropriate treatment (signified by the notes “Pit off,” “O2 6 L/min,” and “side”). Note that fetal heart rate variability was maintained throughout this asphyxial stress, signifying adequate central oxygenation.fetal infection (e.g., chorioamnionitis). In most of these instances, the Classification and Significance offetus is not hypoxic but has an elevated baseline FHR. Baseline Variability It is not uncommon for the FHR baseline to rise in the second stage As described earlier, FHR variability may be absent, minimal, moder-of labor. Certain drugs also cause tachycardia, such as β-mimetic ate, or marked, based on the amplitude range. The moderate (normal)agents used for attempted tocolysis or illicit drugs such as metham- amplitude range is between 6 and 25 beats/min. If the FHR variabilityphetamine and cocaine. is normal, regardless of what other FHR patterns may be present, the Tachycardia should not be confused with the rarer finding of a fetus is not experiencing cerebral tissue acidemia. This is because thefetal cardiac tachyarrhythmia, in which the FHR is faster than 240 fetus is able to centralize the available oxygen and is thus physiologi-beats/min. These arrhythmias may be intermittent or persistent and cally compensated. If excessive hypoxic stress persists, however, thisare the result of abnormalities of the intrinsic determinants of cardiac compensation may break down, and the fetus may have progressiverhythm. Such findings of supraventricular tachyarrhythmias need to hypoxia in cerebral and myocardial tissues. In such cases, the FHRbe monitored closely and possibly treated with medical therapy or variability decreases and eventually is lost.delivery, because they may be associated with deterioration of the fetal There are several possible nonhypoxic causes of decreased or absentstatus. FHR variability:
  12. 12. 408 CHAPTER 22 Intrapartum Fetal Surveillance FIGURE 22-3 No variability of fetal heart rate. The mother had severe preeclampsia and was receiving magnesium sulfate and narcotics. The normal scalp blood pH (7.28) ensures that the absence of variability is nonasphyxic in origin and that the fetus is not chronically asphyxiated and decompensating. The uterine activity channel has an inaccurate trace in the first half. FIGURE 22-4 Unremitting fetal bradycardia. This tracing does not signify asphyxia, because this fetus had complete heart block, with a ventricular rate of about 55 beats/min. Note the absence of fetal heart rate variability. There were serious cardiac structural defects, and the fetus died shortly after birth.1. Absence of the cortex (anencephaly) Reflex late deceleration is sometimes seen when an acute insult (e.g.,2. Narcotized or drugged higher centers (e.g., by morphine, meperi- reduced uterine blood flow resulting from maternal hypotension) is dine, diazepam) (Fig. 22-3) superimposed on a previously normally oxygenated fetus in the pres-3. Vagal blockade (e.g., by atropine or scopolamine) ence of contractions. These late decelerations are caused by a decrease4. Defective cardiac conduction system (e.g., complete heart block) in uterine blood flow (with the uterine contraction) beyond the capac- (Fig. 22-4) ity of the fetus to extract sufficient oxygen. The relatively deoxygenated blood is carried from the fetal placenta through the umbilical vein toPeriodic Changes in Fetal Heart Rate the heart and is distributed to the aorta, neck vessels, and head. Here, LATE DECELERATIONS the low PO2 is sensed by chemoreceptors, and neuronal activity results Late decelerations (Fig. 22-5) are of two varieties: reflex and in a vagal discharge, which causes the transient deceleration. The decel-nonreflex.4,71-73 eration is presumed to be “late” because of the circulation time from
  13. 13. CHAPTER 22 Intrapartum Fetal Surveillance 409 FIGURE 22-5 Late decelerations. These were recorded via Doppler ultrasound in the antepartum period in a severely growth-restricted (1700-g) term infant born to a 32-year-old preeclamptic primipara. Delivery was by cesarean section because neither a direct fetal electrocardiogram nor a fetal blood sample could be obtained due to a firm closed posterior cervix. The infant subsequently did well. FIGURE 22-6 Reflex late decelerations. The fetal heart rate pattern was previously normal, but late decelerations appeared after severe maternal hypotension (70/30 mm Hg), which was a result of sympathetic blockade caused by a caudal anesthetic agent.the fetal placental site to the chemoreceptors and because the progres- death.74 The animals were initially observed with normal blood gases,sively decreasing PO2 must reach a certain threshold before vagal activ- normal FHR variability, presence of accelerations, and no persistentity occurs. There may also be baroreceptor activity causing the vagal periodic changes. After a variable period of time, they first demon-discharge.71 Between contractions, oxygen delivery is adequate and strated late decelerations and retained accelerations. This period wasthere is no additional vagal activity, so the baseline FHR is normal. associated with a small decline in ascending aortic PO2, from 28 toThese reflex late decelerations are accompanied by normal FHR 24 mm Hg, and a normal acid-base state. These late decelerations werevariability and thus signify normal central nervous system integrity probably of the vagal reflex type caused by chemoreceptor activity. At(i.e., the fetus is physiologically “compensated” in the vital organs) an average of more than 3 days after the onset of these reflex decelera-(Fig. 22-6). tions, accelerations were lost in the presence of worsening hypoxia The second type of late deceleration results from the same initial (PO2, 19 mm Hg) and acidemia (pH, 7.22). Fetal death followed anmechanism, except that the deoxygenated bolus of blood from the average of 36 hours of persistent late decelerations, and these latterplacenta is presumed to be insufficient to support myocardial action. decelerations without accelerations were presumed to be of the non-Thus, for the period of the contraction, there is direct myocardial reflex myocardial depression type.hypoxic depression (or failure) and vagal activity.71,73 These nonreflex When late decelerations are present, one should make efforts tolate decelerations are seen without variability (Fig. 22-7), signifying optimize placental blood flow and maternal oxygenation and ensurefetal “decompensation” (i.e., inadequate fetal cerebral and myocardial that maternal blood pressure is normal.oxygenation). They are seen most commonly in states of decreasedplacental reserve (e.g., preeclampsia, intrauterine growth restriction) VARIABLE DECELERATIONSor after prolonged hypoxic stress (e.g., a long period of severe reflex Variable decelerations (Fig. 22-8), have the followinglate decelerations). characteristics: Further support for the two etiologic mechanisms of late decelera-tions comes from observations on chronically catheterized fetal 1. They are variable in duration, depth, and shape.monkeys in spontaneous labor during the course of intrauterine 2. They are usually abrupt in onset and cessation.
  14. 14. 410 CHAPTER 22 Intrapartum Fetal Surveillance FIGURE 22-7 Nonreflex late decelerations with virtual absence of fetal heart rate (FHR) variability. The decelerations represent transient asphyxic myocardial failure as well as intermittent vagal decreases in heart rate. The lack of FHR variability also signifies decreased cerebral oxygenation. Note the acidemia in fetal scalp blood (7.07). The infant, a 3340-g girl with Apgar scores of 3 (1 minute) and 4 (5 minutes) was delivered soon after this tracing. Cesarean section was considered to be contraindicated because of a severe preeclamptic coagulopathy. FIGURE 22-8 Variable decelerations. Intrapartum recording using fetal scalp electrode and tocodynamometer. The spikes in the uterine activity channel represent maternal pushing efforts in the second stage of labor. The normal baseline variability between contractions signifies normal central oxygenation despite the intermittent hypoxic stress represented by the moderate variable decelerations.3. They are not reassuring when there is either a slow return to base- significant period), further diagnostic steps or delivery may be indi- line, a rise in baseline, or an absence of variability in the baseline cated. Certain patterns are of such a severe character that immediate between decelerations. delivery is warranted if they cannot rapidly be relieved (Figs. 22-9 and 22-10). EFFECT OF IN UTERO TREATMENT Fetal oxygenation can be improved, acidemia relieved, and variant Other PatternsFHR patterns abolished by certain modes of treatment. The events that SINUSOIDAL PATTERNresult in fetal stress (recognized by FHR patterns) are presented in The sinusoidal pattern is a regular, smooth, sine wave–like baseline,Table 22-10 together with the recommended treatment maneuvers and with a frequency of approximately 3 to 6 cycles per minute and anpresumed mechanisms for improving fetal oxygenation. These should amplitude range of up to 30 beats/min. The regularity of the wavesbe the primary maneuvers carried out; if the hypoxic event is acute distinguishes this pattern from long-term variability complexes, whichand the fetus was previously normoxic, there is an excellent chance that are crudely shaped and irregular. Another distinguishing feature is thethe undesired FHR pattern will be abolished. absence of beat-to-beat or short-term variability (Fig. 22-11). If the FHR pattern cannot be improved (i.e., if the stress patterns The sinusoidal pattern was first described in a group of severelyindicative of peripheral tissue or central tissue hypoxia persist for a affected Rh-alloimmunized fetuses but was subsequently noted in
  15. 15. CHAPTER 22 Intrapartum Fetal Surveillance 411TABLE 22-10 INTRAUTERINE TREATMENT FOR VARIANT FETAL HEART RATE (FHR) PATTERNSCauses Possible Resulting FHR Patterns Corrective Maneuver MechanismHypotension (e.g., supine Bradycardia, late decelerations Intravenous fluids, position change, Return of uterine blood flow hypotension, conduction ephedrine toward normal anesthesia)Excessive uterine activity Bradycardia, late decelerations Decrease in oxytocin, lateral position Same as aboveTransient umbilical cord Variable decelerations Change in maternal position (e.g., Presumably removes fetal part compression left or right lateral, Trendelenburg) from cord Amnioinfusion Relieves compression of cordHead compression Early or variable decelerations Push only with alternate Allows fetal recovery contractionsDecreased uterine blood flow Late decelerations Change in maternal position (e.g., Enhancement of uterine blood associated with uterine left lateral or Trendelenburg) flow toward optimum contraction Tocolytic agents (e.g., terbutaline) Decrease in contractions or toneProlonged asphyxia Decreasing FHR variability* Change in maternal position (e.g., Enhancement of uterine blood left lateral or Trendelenburg), flow to optimum, increase establishment of maternal in maternal-fetal oxygen hyperoxia gradient*During labor, this is virtually always preceded by a heart rate pattern signifying asphyxial stress (e.g., late decelerations, usually severe), severevariable decelerations, or a prolonged bradycardia. This is not necessarily so in the antepartum period, before the onset of uterine contractions. FIGURE 22-9 Sinister heart rate pattern in a 28-week fetus (gestational age determined after delivery) with baseline tachycardia, absence of heart rate variability, and severe periodic changes. The scalp blood pH was 7.0, and the fetus died shortly after this tracing was made. Cesarean section was not performed because the fetus was believed to be previable, although in fact it weighed 1100 g. There is much artifact in the uterine activity channel. FIGURE 22-10 Bradycardia resulting from cord prolapse. The infant was delivered by cesarean section and did well.
  16. 16. 412 CHAPTER 22 Intrapartum Fetal Surveillance A B FIGURE 22-11 Sinusoidal pattern. A and B, Sinusoidal pattern in a term fetus with severe hemolysis caused by Rh disease. Cord hematocrit was 20%, and the infant, delivered by cesarean section, was subsequently normal. Recording by direct fetal electrode.association with fetuses that were anemic for other reasons and in or lower. Many severely anemic Rh-affected fetuses do not have aseverely depressed infants. It was also described in cases of normal sinusoidal pattern but rather have a rounded, blunted pattern, andinfants born without depression or acid-base abnormalities, but in accelerations are usually absent.these cases there is dispute about whether the patterns were truly If a sinusoidal pattern is seen in an Rh-sensitized patient and severesinusoidal or whether, because of the moderately irregular pattern, hemolysis is confirmed (by peak systolic velocity measurement of flowthey were variants of long-term variability. Such patterns, often called in the middle cerebral artery of the fetus, by cordocentesis, or by thepseudosinusoidal, may also be seen after administration of narcotics deviation in optical density at 450 nm determination by spectropho-to the mother. tometry of amniotic fluid), rapid intervention is needed. This step may It is believed that an essential characteristic of the sinusoidal pattern take the form of delivery or intrauterine transfusion, depending onis extreme regularity and smoothness. Murata and colleagues75 impli- gestational age and the fetal status (see Chapter 26).cated arginine vasopressin in the sinusoidal pattern. The presence of a Management of a sinusoidal pattern in the absence of alloimmu-sinusoidal pattern or variant of this in an Rh-sensitized patient usually nization is somewhat more difficult to recommend. If the pattern issuggests anemia with a fetal hematocrit value of less than 30%. The persistent, monotonously regular, and unaccompanied by short-termpresence of hydrops in such a fetus suggests a fetal hematocrit of 15% variability and cannot be abolished by the maneuvers just described,