What is fetal distress? J. T.

Parer, MD, PhD, and E. G. Livingston, MD

San Francisco, California Fetal distress is a widely used but poorly defined term. This confusion of definition compounds the difficulty of making an accurate diagnosis and initiating appropriate treatment. The fetus reacts at the onset of asphyxia with a remarkable series of responses, primarily a complexly regulated redistribution of blood flow that serves to limit the deleterious effects of oxygen limitation in vital organs. This enables the fetus to survive asphyxia intact unless the insult is profound or prolonged. The most common asphyxial stresses imposed on the fetus during labor are insufficiency of uterine blood flow, or insufficiency of umbilical blood flow, and occasionally decrease in uterine arterial oxygenation. Each of these stresses produces characteristic fetal heart rate patterns: late decelerations, variable decelerations, or prolonged bradycardia. There is strong evidence that the presence of normal fetal heart rate variability represents normal central nervous system integrity, including adequate oxygenation. A decrease or loss of variability in the presence of these patterns is a sign that the physiologic compensations are overwhelmed as a result of the severity of asphyxia. Knowledge of the fetal responses to asphyxia, together with the known evolution of fetal heart rate patterns during asphyxia, should allow a more accurate definition of the onset of unacceptable asphyxia, and more rational management and timing of intervention. (AM J CasTET GVNECOL 1990;162: 1421-7.)

Key words: Asphyxia, fetal distress, fetal heart rate monitoring, fetal physiology The term fetal distress is widely used as an indication for cesarean section, or as justification for midforceps delivery. It is often prefaced by the term acute or chronic. Some authors have defined it as "late decelerations," "severe variable decelerations," or "tachycardia with total loss of short-term variability" of the fetal heart rate.l. Z Others believe that fetal acidosis is necessary to define fetal distress, or they imply that a depressed Apgar score is required. 3 Most physicians recognize that fetal distress is related to asphyxia, with the implication that it should be avoided. We, and others! believe that fetal distress is a poorly defined term, and that this diffuseness of understanding is a disservice to obstetrics. We believe that the term can be more accurately defined with our current understanding of fetal cardiorespiratory responses during labor, and that a better understanding of the pathophysiology of asphyxia will result in improved management of the fetus during labor.

Asphyxia and fetal morbidity Asphyxia has the pathologic meaning of insufficiency or absence of exchange of the respiratory gases, alFrom the Department of Obstetrics, Gynecology and Reproductive Sciences and the Cardiovascular Research Institute, University of California San Francisco. Presented at the Fifty-sixth Annual Meeting of the Pacific Coast Obstetrical and Gynecological Society, Coronado, California, September 17-21,1989. Reprint requests: Julian T. Parer, MD, PhD, Department of Obstetrics, Gynecology and Reproductive Sciences, HSE 1462, University of California San Francisco, San Francisco, CA 94143. 6/6119909

though etymologically it is derived from the Greek word meaning pulseless. Its severity is described in terms of acidosis, hypoxemia, and hypercarbia. With prolonged hypoxia, anaerobic metabolism within the organism results in lactic acidemia, which aggravates the acidosis. In a strict sense all fetuses are born "asphyxiated" because there is a mixed respiratory and metabolic acidosis and hypoxemia in newborns with a totally normal intrapartum course and outcome. In a series of 899 fetuses, at birth the mean umbilical arterial pH was 7.2 (SD ± 0.08) and base excess - 8.3 mmollL (SD ± 4.0).3 The carbon dioxide tension calculated from these means is 49 mm Hg. This "asphyxia" is mild in nature and is not considered a pathologic condition. Such blood gas levels at birth may even be physiologic, to ensure the rapid assumption of the adult circulation and respiration. It is noteworthy that the range of normality calculated as mean - 1 SD is extreme, including a pH as low as 7.12, and base excess to -12 mmoliL. Severe fetal asphyxia can cause cerebral palsy and lesser degrees of neurologic damage, although it is now clear that the proportion of cerebral palsy caused by birth asphyxia is relatively small, perhaps less than 10%.5,6 The degree of damage to any individual fetus after severe asphyxia can be quite variable. For example, some fetuses may not survive the episode in utero, others have central damage that results in a surviving newborn with neurologic defects, and still others survive without apparent deficits. 7. 9 At one end of the scale, we have reasonably good evidence for the limits of fetal tolerance for complete



Parer and Livingston

absence of oxygen delivery. MyerslO showed that after complete cessation of fetal oxygen delivery, hypoxemia and both respiratory and metabolic acidosis occurred rapidly. Intact survival generally did not occur after 10 minutes of oxygen deprivation. Survivors generally had brain stem lesions, although the patterns of damage were variable. If oxygen delivery was prevented for 25 minutes, fetuses could be resuscitated but apparently the hypoxic damage to numerous organs including the heart was so severe that death occurred within a short time. Myers et al. lO -12 have also studied prolonged partial asphyxia in sheep and monkeys as a result of a variety of mechanisms. As with brief complete asphyxia, they found a variable pattern of response. Survivors generally had neurologic deficts as a result of cortical lesions, in contrast to those subjected to complete oxygen cessation. Prolonged partial asphyxia in the above studies has been difficult to define, probably because of the several components, such as degree of hypoxemia, duration, and initial condition of the fetus. Although several other workers have attempted to relate fetal asphyxia to electro physiologic or histologic effects on the brain,13-16 the majority of studies of fetal asphyxia have concerned fetal physiologic responses, including cerebral oxygen uptake to brief periods of asphyxia without benefits of electrophysiologic, pathologic, or behavioral follow_up.17-22 We believe that ideally it is better to quantitate severity of asphyxia by such measures as adequacy of cerebral or myocardial oxygenation. Currently there is no linkage of the pathophysiologic quantification of asphyxia with electrophysiologic consequences that signify unacceptable damage. The production of cerebral damage under controlled physiologic conditions has proved to be difficult. It is known that asphyxia sufficient to result in a preductal arterial oxygen content below 1 mmollL usually is associated with reduced cerebral blood flow and oxygen uptake. 23 However, such asphyxia does not necessarily result in irreversible electrocorticographic changes, or cause neuronal necrosis.24 The fetus is apparently able to temporarily lower its cerebral metabolism by various compensatory mechanisms. 25 There are strong suggestions from the literature regarding newborns that hypotension is necessary for cerebral damage, but this is not unequivocally demonstrated for the fetus. It seems evident, however, that minor or brief periods of asphyxia per se do not cause cerebral damage. The insult must be profound and prolonged,7-9 but the quantitative details have not yet been established. If all infants are born with at least "physiologic" asphyxia, and in the extreme case severe asphyxia causes brain damage, how then can we recognize the transition zone? It is clearly important to recognize the transition because if obstetric intervention occurs too early, it may

June 1990 Am J Obstet Gynecol

be inappropriate, or if too late, the fetus may be damaged. A tentative definition of fetal distress follows: persistent fetal asphyxia that, if not corrected or circumvented, will result in permanent neurologic damage or death. This is not a particularly valuable working definition unless clinical markers of impending or actual fetal neurologic damage can be defined. Fetal responses to asphyxia

There have been many recent studies of fetal responses to oxygen limitation provoked by various means, including reduced uterine and umbilical blood flows. 26 It is now well established that a number of important cardiorespiratory adjustments occur during hypoxia or asphyxia to preserve the oxygenation of certain "priority" organs. Initially there is a selective vasoconstriction of certain organs and vasodilatation of others, which results in an increased blood flow to the brain, heart, and adrenal gland, retention of blood flow to the placenta, and decreases in blood flow to the other organs or areas of the body.27, 28 The overall cardiac output remains fairly stable at moderate degrees of hypoxia, but at more severe degrees of hypoxia or asphyxia cardiac output decreases. 29, 30 A further compensatory response is that overall fetal oxygen consumption declines to values as low as 50% of control. 31 This level can be maintained for periods of up to 45 minutes and is completely reversible on cessation of hypoxia. It is thought that this represents a decrease in oxygen consumption in those vascular beds where circulation is inadequate. There is gradual development of a metabolic acidosis, primarily as a result of the accumulation oflactate. 32 This probably represents anaerobic glycolysis in those vascular beds where oxygen supply is limited. Numerous mechanisms responsible for these hemodynamic alterations have been identified. These include oxygen levels,l7, 33 carbon dioxide tension,34 0:adrenergic activity," p-adrenergic activity,'6 arginine vasopressin,37 endogenous opioids,38 and prostaglandins. 39 There are undoubtedly other as yet unidentified mechanisms. When asphyxia becomes severe, these protective mechanisms are overwhelmed, and there is intense vasoconstriction of all vascular beds. 29 At such degrees of hypoxia, blood flow to and, therefore, oxygen consumption of all organs, including those previously favored, most likely decreases. Cerebral and myocardial oxygen consumption can be maintained during moderate hypoxia by the increase in blood flow to the respective organ that exactly balances a decrease in arteriovenous oxygen content difference. 17.40 However, at more severe degrees of asphyxia, when an adequate compensatory increase in blood flow to the organs no

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longer occurs, the oxygen consumption can no longer be maintained.""' 23 This represents a point of decompensation of the physiologic mechanisms that had previously lessened the impact of relatively shon periods of asphyxia on fetal vital organs. This stage most likely precedes the final bradycardia, hypotension, and death by a relatively shon time. It is thought that hypoxic organ damage occurs during this phase. However, such observations do not assist in recognition of the degree of oxygen consumption deficit that can be tolerated before permanent damage occurs. This will require a combination of metabolic, electrophysiologic and pathologic studies. Prognostic capacity of FHR variability

It was commonly stated in the past that fetal heart rate monitoring is extremely accurate in diagnosing fetal vigor when the pattern is normal, but that it is poor for determining depression when the pattern is "abnormal. "41 4" That is, its specificity, or ability to correctly diagnose normal, was thought to be poor. This resulted in the overdiagnosis of "fetal distress," and at times unnecessary intervention leading to either cesarean section or potentially traumatic operative vaginal deliveries. We believe that this may be true if fetal heart rate (FHR) patterns are interpreted according to older concepts that considered the prominent "abnormality" to be decelerations of FHR with contractions. Empirical clinical evidence strongly suggests that the addition of the determination of FHR variability to the FHR pattern interpretation can aid in improving specificity. Evidence for this view has taken the form of clinical observations 43 or retrospective surveys of outcome after monitoring. H . 46 The common trend in these studies is that the presence of FHR variability is almost invariably associated with fetal vigor at birth, even in the presence of various decelerations or bradycardias. A further observation is that of infants who died in utero while being monitored, none had the presence of normal FHR variability!7 The corollary of this observation is that if the FHR has normal variability, the fetus is at low risk for immediate death caused by asphyxia. The preceding observations and widespread clinical experience have resulted in the acceptance of FHR variability by many clinicians as a prime indicator of fetal vigor!7 The acceptance of the efficacy of this approach to FHR interpretation is not, however, universal,48.5o and we believe that the overdiagnosis of the "asphyxiated" fetus will continue until a physiologic basis for FHR variability is demonstrated, leading to more rational interpretation. The original interpretation of FHR patterns stressed the decelerations (late or variable decelerations) occurring with contractions, and equated their presence to "fetal distress," which then


dictated operative intervention.">! The alternative interpretation states that the decelerations, or bradycardias, indicate intermittent asphyxial "stresses" (generally insufficiency of uterine or umbilical blood How), whereas the collective influence of these stresses on the fetal physiologic compensatory mechanisms is determined by the decrease or loss of FHR variability, signifying a cumulative oxygen debt and decompensation!' Thus the presence of FHR variability indicates central (nervous system, myocardial, or both) normoxia, whereas its decrease in the presence of the stress patterns indicates a decrease in the oxygenation of these organs. It has long been recognized that FHR variability can be affected by numerous influences other than asphyxia. Such influences include congenital anomalies and drugs, and in some cases there is no apparent cause, although the infant is normal at birth. Examples of some factors responsible for decreased or absent variability include anencephaly, complete heart block, narcotic administration (presumably acting on the central nervous system), and atropine administration (presumably blocking oscillatory influences transmitted by the vagus nerve).2" The source ofFHR variability is clearly complex, with inputs from many cycling physiologic phenomena. including respiratory arrhythmia, blood pressure fluctuations, and thermoregulation, at least in the adult. 52 However, many of the observations are most consistent with the theory that the presence of normal variability requires integrity of (I) the cerebral cortex, (2) the midbrain, (3) the vagus nerve, and (4) the cardiac conduction system. 47 It is known that different fetuses have an intrinsic "quantity" of variability, and also that this can change with differences in fetal state. 5355 It is also known that the components used to describe fetal state can be altered by hypoxia or hypercapnia 56 and by short periods of decreased uterine blood flow. 57 58 Again, the presence of certain state variables can affect others; for example, during fetal breathing movements there is a respiratory arrhythmia,'9 and during prelabor myometrial activity there is a change to the quiescent state in fetal sheep.50 It is important to be aware of such activities to make the appropriate distinction between asphyxial and nonasphyxial causes of decreased variability. Clinical implications

There are basically three common means by which the human fetus can become asphyxiated (or hypoxic); (1) insufficiency of uterine blood flow,"" (2) insufficiency of umbilical blood flow,61.62 or (3) a decrease in maternal anerial oxygen content. 3 ! Other mechanisms, for example, fetal anemia or increased fetal oxygen needs (in pyrexia), are relatively rarely seen clinically.


Parer and Livingston

In clinical obstetrics these three common mechanisms can be recognized during labor (that is, in the presence of uterine contractions) by various FHR patterns. Uterine contractions are thought to cause the transient decelerations because of the concomitant decrease in uterine blood flow with the contraction,5!,63 or an associated decrease in umbilical blood flow (e.g., as a result of umbilical cord compres~ion5!). The patterns corresponding to the above mechanisms are late decelerations, variable decelerations, and persistent fetal bradycardia!7 A prolonged stepwise insufficiency of uterine or umbilical blood flow would likewise be recognized as a bradycardia. It has been proposed that a fetus with normal FHR variability will not revert to one with absent FHR variability caused by asphyxia during labor unless one of these asphyxial "stress" patterns is present!7 Conversely, if the FHR variability is absent on initial application of the FHR monitor, then it is not possible to distinguish between asphyxial and nonasphyxial causes of decreased FHR variability, and the fetal stimulation test or fetal blood sampling for determination of acid-base status must be performed. On the basis of the above considerations, a tentative definition of fetal distress is as follows: progressive fetal asphyxia that, if not corrected or circumvented, will result in decompensation of the physiologic responses (primarily redistribution of blood flow to preserve oxygenation of vital organs) and cause permanent central nervous system and other damage or death. The clinical means by which we currently use the above definition to ensure adequate fetal compensation is by noting the progress of severity of the FHR stress patterns, and the retention of FHR variability. Intermittent or sustained decreases in FHR variability in the presence of stress patterns are assumed to signal the onset of decompensation, unless asphyxia is ruled out by ancillary testing. There may be a role for fetal blood sampling, but in the presence of normal FHR variability its role is quite limited. 64 ,65 It is hoped that future physiologic studies, and correlation with FHR patterns, will further refine the definition of "fetal distress" and make the diagnosis more accurate in the clinical setting. REFERENCES 1. Haverkamp AD, Orleans M, Langendoerfer S, McFee], Murphy], Thompson HE. A controlled trial of the differential effects of intrapartum fetal monitoring. AM ] OBSTET GYNECOL 1979;134:399-408. 2. Haesslein HC, Niswander KR. Fetal distress in term pregnancies. AM] OBSTET GYNECOL 1980;137:245-53. 3. Sykes GS, Johnson P, Ashworth F, et al. Do Apgar scores indicate asphyxia? Lancet 1982; 1:494-6. 4. Steer P. Has the expression "fetal distress" outlived its usefulness? Br] Obstet Gynaecol 1982;89:690-3. 5. Nelson K. What proportion of cerebral palsy is related to birth asphyxia? ] Pediatr 1988; 112:572-4. 6. Blair E, Stanley FJ. Intrapartum asphyxia: a rare cause of cerebral palsy.] Pediatr 1988;112:515-9.

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7. Freeman ]M, Nelson KB. Intrapartum asphyxia and cerebral palsy. Pediatrics 1988;82:240-9. 8. Paneth N, Stark R. Cerebral palsy and mental retardation in relation to indicators of perinatal asphyxia. AM] OBSTET GYNECOL 1983;147:960-6. 9. Low]M, Gaibraith RS, Muir DW, et al. Motor and cognitive deficits after intrapartum asphyxia in the mature fetus. AMJ OBSTET GYNECOL 1988;158:356-61. 10. Myers RE. Two patterns of perinatal brain damage and their conditions of occurrence. AM .I OBSTET GYNECOL 1972;112:246-76. II. Myers RE, Beard R, Adamson K. Brain swelling in the newborn rhesus monkey following prolonged partial asphyxia. Neurology 1969;19:1012-8. 12, Brann AW, Myers RE. Central nervous system findings in the newborn monkey following severe in utero asphyxia. Neurology 1975;25:327-38. 13. Mann LI. Effect of hypoxia on fetal cephalic blood flow, cephalic metabolism and EEG. Exp Neurol 1970;29:33648. 14. Clapp .IF III, Mann LJ, Peress NS, Szeto HH. Neuropathology in the chronic fetal lamb preparation: structurefunction correlates under different environmental conditions. AM .I OBSTET GYNECOL 1981; 141 :973-86, 15. Hill A, Volpe JJ. Hypoxic-ischemic brain injury in the newborn. Semin Perinatol 1982;6:25-41. 16. Ting P, Yamaguchi S, Bacher ]D, et al. Hypoxic-ischemic cerebral necrosis in midgestational sheep fetuses: physiologic correlations. Exp Neurol 1983;80:227-45. 17. Jones MD ] r, Sheldon RE, Peeters LL, et al. Fetal cerebral oxygen consumption at different levels of oxygenation. ] Appl Physiol 1977;43:1080-4. 18. Lou HC, Lassen NA, Tweed WA, et al. Pressure passive cerebral blood flow and breakdown of the blood-brain barrier in experimental fetal asphyxia. Acta Paediatr Scand 1979;68:57-63. 19. Johnson GN, Palahniuk R], Tweed WA, et al. Regional cerebral blood flow changes during severe fetal asphyxia produced by slow partial umbilical cord compression. AM ] OBSTET GYNECOL 1979;135:48-52. 20. Ashwal S, Majcher ]S, Vain N, Longo LD. Patterns offetal lamb regional cerebral blood flow during and after prolonged hypoxia. Pediatr Res 1980; 14: 1104-1 O. 21. Tweed WA, Cote .I, Pash M, Lou H. Arterial oxygenation determines autoregulation of cerebral blood flow in the fetal lamb. Pediatr Res 1983; 17:246-9. 22. Richardson B, Rurak D, Patrick], Homan], Carmichael L. Cerebral oxidative metabolism during sustained hypoxaemia in fetal sheep . .I Dev Physiol 1989; II :37-43. 23. Field DR, Parer .IT, Auslender RA, Cheek DB, Baker W, .I ohnson J. Cerebral oxygen consumption during asphyxia in fetal sheep . .I Dev Physiol [In press]. 24. Gunn AJ, Parer .IT, Mallard C, Gluckman PD. Cerebral histological damage following acute reduction of uterine blood flow in fetal sheep. In: Abstracts of scientific papers. Sixteenth annual conference, Society for the Study of Fetal Physiology. Reading, United Kingdom: July 1989:C1. 25. Richardson BS, Patrick ]E, Abduljabbar H. Cerebral oxidative metabolism in the fetal lamb: relationship to electrocortical state. AM] OBSTET GYNECOL 1985; 153:426-31. 26. Court D], Parer ]T. Experimental studies of fetal asphyxia and fetal heart rate interpretation. In: Nathanielsz PW, Parer ]T, eds. Research in perinatal medicine. New York: Perinatology Press, 1984 vol 1:113. 27. Cohn HE, Sacks EJ, Heymann MA, Rudolph AM. Cardiovascular responses to hypoxemia and acidemia in fetal lambs. AMJ OBSTET GYNECOL 1974;120:817-24. 28. Peeters LLH, Sheldon RE, Jones MD, et al. Blood flow to fetal organs as a function of arterial oxygen content. AM ] OBSTET GYNECOL 1979;135:637-46. 29. Yaffe H, Parer ]T, Block BS, Llanos AJ. Cardiorespiratory responses to graded reductions in uterine blood flow iIi the sheep fetus. J Dev Physiol 1987;9:325-36.

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30. Cohn HE, Piasecki GJ, Jackson BT. The effect of fetal heart rate on cardiovascular function during hypoxemia. AM J OBSTE1' GVNECOL 1980; 138: 1190-9. 31. Parer JT. The effect of acute maternal hypoxia on fetal oxygenation and the umbilical circulation in the sheep. Eur J Obstet Gynecol Reprod Bioi 1980; 10: 125-36. 32. Mann L. Effects of hypoxia on umbilical circulation and fetal metabolism. AmJ PhysioI1970;218:1453-8. 33. Jones MD, Sheldon RE, Peeters LL, et al. Regulation of cerebral blood flow in the ovine fetus. Am J Physiol 1978;235:H 162-166. 34. Rosenberg AA,Jones MD, Traystman RJ, et al. Response of cerebral blood flow to changes in Pc02 in fetal, newborn, and adult sheep. AmJ PhysioI1982;242:H862-866. 35. Reuss ML, Parer JT, Harris JL, Krueger TR. Hemodynamic effects of alpha-adrenergic blockade during hypoxia in fetal sheep. AM J OBS1'ET GYNECOL 1982;142: 410-5. 36. Court DJ, Parer JT, Block BSB, Llanos AJ. Effects of betaadrenergic blockade on blood flow distribution during hypoxemia in fetal sheep. J Dev Physiol 1984;6:349-58. 37. Perez R, Espinoza M, Riquelme R, Parer JT, Llanos AJ. Arginine vasopressin mediates some of the cardiovascular responses to hypoxemia in fetal sheep. Am J Physiol 1989;256: 1011-8. 38. Espinoza M, Riquelme R, Germain AM, Tevah J, Parer JT, Llanos AJ. Role of endogenous opioids in the cardiovascular responses to asphyxia in the fetal sheep. Am J Physiol 1989;256:RI063-RI068. 39. Auslender RA, Arnold SA, Parer JT, Glosten B, Johnson J, Preston P. The effects of meclofenamate on fetal hemodynamics during hypoxia. In: Jones CT, ed. Proceedings of the International Symposium on Foetal and Neonatal Development, Oxford, 1987. New York: Perinatology Press, 1988:353-6. 40. Fisher DJ, Heymann MA, Rudolph AM. Fetal myocardial oxygen and carbohydrate consumption during acutely induced hypoxemia. Am J Physiol 1982;242: H657-H661. 41. Hon EH. Detection of fetal distress. In: Wood C, ed. Proceedings of the Fifth World Congress of Gynecology and Obstetrics. Melbourne: Butterworth, 1967. 42. Schifrin BS, Dame L. Fetal heart rate patterns: prediction of Apgar score.JAMA 1972;219:1322-5. 43. Boehm FH. FHR variability: key to fetal well-being. Contemp Obstet Gynecol 1977;9:57-68. 44. Hammacher K, Huter KA, Bokelmann J, Werners PH. Foetal heart frequency and perinatal condition of foetus and newborn. Gynaecologia (Basel) 1968;166:348-60. 45. Krebs HB, Petres RE, Dunn LJ, et al. Intrapartum fetal heart rate monitoring: I. Classification and prognosis of fetal heart rate patterns. AM J OBSTET GYNECOL 1979; 133:762-72. 46. Paul RH, Suidan AK, Yeh S, Schifrin BS, Hon EH. Clinical fetal monitoring: VII. The evaluation and significance of intrapartum baseline FHR variability. AM J OBSTET GyNECOL 1975;123:206-10. 47. Parer JT. Handbook of fetal heart rate monitoring. Philadelphia: WB Saunders, 1983. 48. Haverkamp AD, Orleans M, Langendoerfor S, et al. A controlled trial of the differential effects of intrapartum fetal monitoring. AM J OBSTET GYNECOL 1979; 134:399408. 49. MacDonald D, Grant A, Sheridan-Pereira M, et al. The Dublin randomized controlled trial of intrapartum fetal heart rate monitoring. AM J OBSTE1' GYNECOL 1985; 152:524-39. 50. Leveno KJ, Cunningham FS, Nelson S, et al. A prospective comparison of selective and universal electronic monitoring in 34,995 pregnancies. N Engl J Med 1986;315: 615-9. 51. Hon EH. An atlas of fetal heart rate patterns. New Haven, Connecticut: Harty Press. 1968.


52. Kitney RI, Rompelman O. The study of heart-rate variability. Oxford, England: Clarendon Press, 1980. 53. Dawes GS, Fox HE, Leduc BM, et al. Respiratory movements and rapid eye movement sleep in the foetal lamb. J PhysioI1972:220:119-43. 54. Martin CB. Behavioral states in the human fetus.J Reprod Med 1981;26:425-32. 55. Nijhuis JG, Prechtl HFR, Martin CB Jr, Bots RSGM. Are there behavioral states in the human fetus? Early Hum Dev 1982;6:177-95. 56. Boddy K, Dawes GS, Fisher R, et al. Foetal respiratory movements, electrocortical and cardiovascular responses to hypoxaemia and hypercapnia in sheep. J Physiol (Lon d) 1974;243:599-618. 57. Harding R, Poore ER, Cohen GL. The effect of brief episodes of diminished uterine blood flow on breathing movements, sleep states and heart rate in fetal sheep. J Dev Physiol 1982;3:231-43. 58. Bocking AD, Harding R. Effects of reduced uterine blood flow on electrocortical activity, breathing, and skeletal muscle activity in fetal sheep. AM J OBSTE1' GYNECOL 1986;154:655-62. 59. Divon MY, Yeh S-Y, Zimmer EZ, et al. Respiratory sinus arrhythmia in the human fetus. AM J OBS1'E1' GYNECOL 1985;151:425-8. 60. Nathanielsz PW, Bailey A, Poore ER, et al. The relationship between myometrial activity and sleep state and breathing in fetal sheep throughout the last third of gestation. AMJ OBSTET GYNECOL 1980;138:653-9. 61. Towell ME, Salvador HS. Intrauterine asphyxia and respiratory movements in the fetal goat. AM J OBSTE1' GyNECOL 1974;118:1124-31. 62. Itskovitz J, LaGamma EF, Rudolph AM. The effect of reducing umbilical blood flow on fetal oxygenation. AM J OBSTET GYNECOL 1983; 145:813-8. 63. Griess FC. Concepts of uterine blood flow. In: Wynn RM, ed. Obstetrics and gynecology annual. New York: Appleton-Century-Crofts, 1973. 64. Parer JT. The current role of intrapartum fetal blood sampling. In: Resnick R, ed. Clinical obstetrics and gynecology. New York: Harper & Row, 1980:565-682. 65. Clark SL, Paul RH. Intrapartum fetal surveillance: the role of fetal scalp blood sampling. AM J OBSTET GYNECOL 1985; 153:717-20.

Editors' note: This manuscript was revised after these discussions were presented. Discussion

Irvine, California. In this article Drs. Parer and Livingston have attempted to define fetal distress by reviewing the fetal physiologic adaptations that occur with decreased oxygenation and serve to protect the brain, heart, and adrenals. The definition that they have developed is a logical one: progressive fetal asphyxia that, if not corrected or circumvented, will result in decompensation of the physiologic responses (primarily a redistribution of blood flow to preserve oxygenization of vital organs) and cause permanent damage to the central nervous system and other damage or death. The difficulty lies in the use of this definition clinically. We know the heart rate change is associated with a change in fetal oxygen (i.e., late, variable, or prolonged decelerations), so we can determine the first half of the definition with continuous heart rate monitoring. The authors would also like us to believe that the second half of the definition, decompensation, can be determined by examining the DR. EDWARDJ. QUILLIGAN,

1426 Parer and Livingston

heart rate variability. Although changes in heart rate variability have been shown to result from hypoxia, I am unaware of studies relating variability to decompensation. Let us assume for a moment that they do reflect decompensation. Will it help clinically? Our goal is to prevent fetal death and damage without unnecessary cost to the mother. I would emphasize the latter without unnecessary cost to the mother because five of the seven randomized trials have demonstrated an increase in the cesarean section rate in the continuously monitored group. I In terms of reduction of intrapartum death, I believe continuous monitoring has accomplished that, even though the trials mentioned above do not prove it. I Nonrandomized trials such as the one by Dr. Yeh et aJ.2 at University of Southern California do show a difference and reveal the large number of patients necessary to demonstrate this difference (about 100,000). I would agree with the authors that combining abnormal fetal heart rate pattern and fetal heart rate variability may reduce this unnecessary cesarean section rate for fetal distress, and still prevent antepartum deaths. It is in the prevention of central nervous system damage that we have difficulty. There is no good evidence in the literature that the frequency of central nervous system damage in infants is decreasing.' In fact, the opposite seems true. Furthermore, as the authors point out, a very small percentage of central nervous system damage is incurred during labor. When we studied infants who had cerebral palsy, there was an increased incidence of abnormal fetal heart rate patterns and absent variability, and there were fetuses in whom cerebral palsy developed without any typical fetal distress patterns.' It appears to me that if we are to reduce central nervous system damage, we need additional information, such as what degree of lack of oxygen for how long causes brain damage? Although we have some information from Myers'5 classic studies, it must be remembered that the study animals were anesthetized or heavily sedated, which may influence the brain's ability to tolerate hypoxia. To further confuse the issue, Clapp et al. 6 have shown that brain damage in fetal sheep can be caused by intermittent cord compression without fetal acidosis. The authors have indicated the final event in fetal decompensation is the reduction in fetal brain blood flow as a result of a decrease in fetal cardiac output. It would be important to know whether the authors think if it is at this point that brain damage occurs. If so, do they see any role for the measurement of blood flow in the umbilical or carotid vessels to assist in determining this point of decompensation? I do not mean to denegrate the role of continuous fetal heart rate monitoring in the management of labor nor the authors' explanation for the development of brain damage. I simply believe that there are a number of "blanks" in the equation at this time, before we can say we have the factual information to significantly reduce that small portion of brain damage that may occur

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during labor. These authors have done excellent work in helping to fill in those blanks, and I would urge them to continue their work. REFERENCES 1. Chalmers I. Randomized controlled trials of intrapartum monitoring. In: Thalhammer 0, Baumgarten KV, Polaka A, eds. Perinatal medicine. Stuttgart: George Thieme, 1979:260-5. 2. Yeh SY, Diaz F, Parel R. Ten-year experience of intrapartum fetal monitoring in Los Angeles County/University of Southern California Medical Center. AM J OBSTET GYNECOL 1982;143:496-500. 3. Hargberg D, Hargberg G, Olow I. The changing panorama of cerebral palsy in Sweden: IV. Epidemiologic trends 1959-1977. Acta Paediatr Scand 1984;73:433-40. 4. Keegan KA Jr, Waffarn F, Quilligan EJ. Obstetric characteristics and fetal heart rate patterns of infants who convulse during the newborn period. AM J OBSTET GYNECOL 1985;153:732-7. 5. Myers RE. Two patterns of perinatal brain damage and their conditions of occurrence. AM J OBSTET GYNECOL 1972;112:246-76. 6. Clapp JF, Peress NS, Wesley M, Mann LI. Brain damage after intermittent partial cord occlusion in the chronically instrumented fetal lamb. AM J OBSTET GYNECOL 1988; 159:504-9.

DR. ROBERT GoODLIN, Denver, Colorado. The term heart rate variability is one that is dear to me. I think I introduced it at this society'S 1970 meeting in Hawaii and Dr. Quilligan was my official discussant. I Like many things that I have done, it seems to have gotten out of hand. On our labor deck, for instance, we often cannot begin oxytocin administration or do certain other procedures because somebody has decided that the fetal heart rate tracing shows decreased variability. Zalar and Quilligan 2 showed that the loss of beat-to-beat variability had no significance. I suggest that there are many papers that show that loss of beat-to-beat variability by itself is a rather useless concept.' I hope that the authors' article will not now carve the concept in stone so that we cannot dig ourselves out of the hole. It seems to me that if you call it asphyxia, you must obtain a fetal blood sample, scalp or otherwise.

REFERENCES 1. Goodlin RC. Intrapartum fetal heart rate responses and plethysmographic pulse. AM J OBSTET GYNECOL 1971; 110:210. 2. Zalar RW Jr, QuilIigan EJ. The influence of scalp sampling on the cesarean section rate for fetal distress. AM J OBSTET GYNECOL 1979;135:239-46. 3. Fleischer A, Schulman H, J agani N, Mitchell J, Randolph G. The development of fetal acidosis in the presence of an abnormal fetal heart rate tracing. I. The average for gestational age fetus. AM J OBSTET GYNECOL 1982; 144:55-60.

DR. PARER (Closing). Dr. Quilligan, you ask if I have solid evidence that loss of FHR variability in an appropriate setting does signify decompensation. I do not have incontrovertible, hard data yet. I think I have provided most of the physiologic data I have and little

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of it is published. We have not closed the circle yet, but I accept as an article of faith that these data will become available. The reason I accept this is the wide clinical experience I had at Los Angeles County Hospital under the guidance of yourself and Dr. Hon. Since that time I have looked for exceptions to the rule "fetuses born with normal heart rate variability will have an Apgar score above 7 at 5 minutes no matter what else is going on with the heart rate." There are very few exceptions to that rule, maybe one in a thousand. When there is heart rate variability, the infants are vigorous at birth. There are more formal data available. Krebs et aI., for example, conducted a study and reached similar conclusions (see reference 4.1». Variability was determined within approximately 30 minutes of birth and the predictability for a vigorous fetus was 98%. This is very good and holds true in the presence oflate and variable deceleration. Your second question, why the incidence of cerebral palsy has not decreased over the years despite our intensive monitoring, is a difficult one. One problem is that intrapartum asphyxia is probably responsible for < 10% of all cerebral palsy. No matter how well we abolish intrapartum asphyxia as a cause of cerebral palsy, we will not alter the overall incidence much. My view on this is that intrapartum asphyxia is a potentially avoidable cause of cerebral palsy; that is why I think we should concentrate our efforts to avoid this problem. As we mentioned in discussion of a previous paper, part of the problem with some controlled trials of fetal monitoring is that the rules for heart rate interpretation were quite different from those accepted today. Two aspects deserve mention. First, there was no emphasis on heart rate variability, and second, response times were not clearly defined. One trial required that the response time be less than 90 minutes in the case of an infant with signs of asphyxia. Now, if we say that an infant can sustain brain damage within 10 minutes, then 90 minutes is totally inappropriate. That is not the fault of electronic fetal monitoring but rather the fault of the obstetric facility that cannot intervene more quickly.

What is fetal distress


Dr. Quilligan, you mentioned a subject I want to emphasize: the degree and duration of asphyxia. There is almost certainly an interaction between duration and degree of asphyxia on the one hand and the previous condition of the fetus (whether or not it has glycogen stores or is growth retarded) on the other. The answer to these questions will quite clearly affect the relationship between asphyxia and brain damage. Dr. Kirschbaum, you would like to call fetal distress asphyxia and we are not far apart on that. You also want to bring dysfunction of other organ systems into the definition and I would be delighted to do that. I agree that other organ dysfunction should ultimately be part of the overall definition of intolerable asphyxia. The difficulty is that in a clinical setting, it is difficult enough to include only the brain. Dr. Goodlin, you pointed out that I did not emphasize sufficiently the fact that we cannot isolate loss of FHR variability. Loss of FHR variability signifies decompensation of physiologic mechanisms only in a particular setting. For simplicity, I will say that if a fetus has a loss of variability during labor in the absence of deceleration or bradycardia, you can be almost 100% sure it is not a result of asphyxia. The setting must be appropriate before you can rationally call a loss of variability the result of asphyxia. You made another point about fetal blood sampling. If you study some of the original papers of fetal blood sampling, you will find that they have a nagging inaccuracy of 10% or 20%; that is, if you do 100 fetal blood samples on normal fetuses during labor, acidosis will be found in about 10 or 20. Thus, if you have obtained a fetal blood sample for whatever reason and proceed to act on the result, these infants at birth would be quite vigorous. The inaccuracy inherent in the interpretation of fetal blood samples far surpasses the inaccuracy in determining FHR variability. The reason is that peripheral blood, which can rapidly turn cyanotic on vasoconstriction, is being sampled. What we need is a central marker of fetal integrity. I believe that FHR variability is the best candidate for that.

What is fetal distress?

Fetal distress is a widely used but poorly defined term. This confusion of definition compounds the difficulty of making an accurate diagnosis and ini...
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