pathophysiological classification of perinatal depressions

24 Takemura, Classification of perinatal depressions

J. Perinat. Med.l (1973) 24

Pathophysiological classification of perinatal depressionsand cybernetics in obstetrics — a wörking hypothesisfor a model of lifeHikatu Takemura

Department of Obstetrics and Gynecology, Osaka University Medical SchoolOsaka, Japan (Head: Prof. K. KURACHI, M.D., Ph. D.)^

Received September 5, 1972. Accepted September 19, 1972.

Since about a decade ago the electronic fetalheart rate (FHR) monitoring developed by severalinvestigators [8, 11, 14, 32] and the fetal capillary-blood analysis (FBA) for the acid-base Statusstudied by SALING [27, 28] and others [2, 20, 36]h^ve both, increased our knowledge of fetaldamage in the perinatal period. Certainly there aresome particularly dangerous conditions to beovercome by a fetus in vaginal delivery. Thispaper describes the author's present classifica-tion of perinatal depressions based on thepathophysiological hypothesis of how a fetus isjeopardized.

1. Presumptions

1.1 A model of fetal circulationA fetus lives a fish's life in utero. His circulationand respiration are not yet so differentiated äs inthe adult into separate respective Systems. So,very simply, the System of fetal circulation andrespiration (oxygenation) is diagrammaticallyshown in fig. 1. The anatomy is rather compli-cated but the function itself is quite simple andprimitive. Placental oxygenation is carried outvia the umbilical circulation which is.the by-pass of the fetal descending aorta, carrying abouthalf of the cardiac output äs DAWES' [9] datasuggest.

1.2 Pathogenesis of two kinds of FHR de-celeration during labor

HON [15] has noted three types of FHR decel-erations: early, late and variable with uterinecontractions (fig. 2), but it is widely known thatonly the last two are clinically important. As

Curriculum vitaeHIKARU TAKEMURA, M. D.& P/J. D.: Lecturer of Ob-stetrics and Gynecology, OsakaUniversity Medical SchooLBorn in Osaka, Japan onMarch 31, 1936, he graduatedfrom Osaka University Medi^cal School in 1961 witb thedegree of M. D. and fromOsaka University GraduateSchool of Medicine in 1966with the degree of P h. D.under the thesis entitled "Stud-ies on fetal EGG informationsin late pregnancy and parturition", by which he was honored äsan Annual Pri%e Winner of Japan Society of Obstetrics andGynecology in 1968. His present interests are focused aroundperinatology, bio-medical engineering and ultrasonic investigationsof the fetus and its environments.

Fig. 1. The simplest model of fetal circulation and itscontrolling mechanisms of the heart rate. U. A. andU. V. are designated for the umbilical arteries and vein.Ch. R. and P. R. mean the chemoreceptors and thepresso- or baro-receptors in the fetus. The umbilical circu-lation cairying out the placental respiration is just a by-passof the fetal corporeal circuits of aorta.

J. Perinat. Med. l (1973)

Takemura, Classification of perinatal depressions 25

early onset early onset early onset

50UC

Head compression

t

Early deceleration (HC)

artery

Uteroplacenta insufficiency Late deceleration (UPI)

Umbical cord compression

180FHR^VVpj., JYV-r 'l l100 m·/ ff i-···'

variable onset variable onset

Variable deceleration (CC)

Fig. 2. HON'S scheme showing threetypes of characteristic FHR decelera-tion with uterine contractions, with theirphysiological mechanisms for each, re-spectively.

illustrated in fig. 2 the variable FHR decelera-tion is thought to be induced by such obstruc-tions of the umbilical circulation äs compres-sion or constriction of the cord vessels. Accordingto the model described in fig. l such a promptFHR deceleration can be satisfactorily explainedby the sudden increase of impedance in theumbilical circulation, which is counteracted byreflex FHR deceleration to keep the bloodpressure normotensive. Because about fifty percent of the total cardiac Output is shut out incases of complete compression of the umbilicalarteries, the FHR must drop from 140 to 70 orbelow within a few beats. The physiologicalexperiments and mathematical models by ROSEN-BLUETH and SIMEONE [26] have shown that suchrapid variations in heart rate can* only beachieved by vagal reflex. The vagus is activatedby various afferent Stimuli, the most importantbeing the baroreceptive Stimuli mediated bypressure sensors, such äs those in the carotidsinus, äs is well documented [5, 13, 18, 19, 34].

In any case, the variability of FHR patterns in"cord" type-decelerations, äs far äs frequency isconcerned, can only be explained by rapid vagalcontrol of heart rate.On the other hand, if we consider increasedimpedance in the other half of fetal circulation,that is, in the fetal corporeal blood flow, it iseasy to understand how the late FHR decelerationoccurs. HON called this a utero-placental in-sufficiency (UPI) pattern of FHR decelerationwith uterine contraction, which means that someimpediments in the uteroplacental circulation maybe the cause of this type of fetal bradycardia.By continuous measurement of PO2 CALDEYRO-BARCIA, POSEIRO, MENDEZ-BAUER and GULIN [7]and WALKER, PHILLIPS, POWE and WOOD [33]showed that some P02 fluctuation quite similarto the UPI pattern occurred in the fetus duringuterine contractions. Therefore, the fetal hypoxiainevitably induced during reasonably intenseuterine contraction is signaled through fetalchemoreceptors (äs reported by PURVERS and

J. Pcrinat. Med. l (1973)


BISCOE [24]) and brings about peripheral vaso-constriction, resulting in the gradual increase ofvascular impedance. This is counteracted by thegradual and delayed slowing of late FHR de-celeration (dip II or UPI). The model in fig. ldescribes this process, enabling us to see how thedynamic dimensions of two types of FHR de-celeration can be differentiated from each other.The induction of UPI is caused not only by asingle loop of baroreceptic control äs in "cord"but also by a chemical loop, via fetal chemo-receptors, which has a longer reaction time. Theprimary, physical emergency reflex in the cir-culation is promptly activated by barorecepticcontrols but the secondary adaptation in hypoxicemergency is a redistribution of blood flow,keeping the central organs such äs brain and

\heart supplied, with some sacrifice to non-vitalorgans such äs skin, intestine and extremities(tab. 1).

Circulatory insufficiency of the placentadue to uterine contraction,

maternal hypotension,exercise of the mother, etc.

Fetal hypoxia

(A) acute fetal distress (B) subacute fetal distress

l <— I Chemoreceptor reflex

Fetal peripheral vasoconstrictionin the skin, extremities, and intestine.

! *— Baroreceptor reflex

Gradual fetal bradycardiato keep the cerebral and coronary blood pressurenormotensive, and probably to save oxygenconsumption äs a whole.

Tab. 1. A hypothetical mechanism of late FHR decelera-tion. Refer to the model of fetal circulation describedin fig. 1.

2. Classification of perinatal depressions

2.1 Acute fetal distress

Upon the basis of a model of fetal circulationand the pathogenesis of fetal bradycardia, it shouldbe easy to understand that there are three differenttypes of fetal distress äs schematically drawn infig. 3. The umbilical blockade of fetal oxygena-tion causes sudden decrease of P02 and rapidretention of carbon dioxide in the fetal blood,

Functional umbilical blockof fetal oxygenation whichcauses mainly "fetal respi-ratory acidosis" that is quitereversible.

(C) chronic fetal distress

Functional utero-placentalblock of fetal oxygenationwhich causes mqstly "fetalcombined acidosis" that isfairly reversible.

Distressed area

Functional matemal blockand/or organtc placentalblock of fetal oxygenationwhich cause mainly "fetalmetabolic acidosis" thatis poorty reversible.

Fig. 3. Schematic presenta-tion of three types of fetaldistress with their pathogen-eses in the f requency äs well ässpatial domains, respectively.

which in turn brings about acute, primaryrespiratory acidosis of the fetus.Such a typical case is presented in fig. 4, which showsprolonged marked fetal bradycardia (almost äs slow äs60 bpm) of about five minutes duration just before deli-very. The FBA Po2 was lowered from 20 to 2 mmHgand Pco2 was raised from 38 to 63 mmHg. The fetal aci-dosis of pH 7.15 is respiratory rather than metabolic.Although the acidosis of the umbilical blood was not sopronounced äs in the last FBA specimen, the greatarterio-venous differences in pH and in Po2 and Pco2are good etiological evidence för the presence of blockadein the umbilical circulation. The infänt was' born with aslight depression of 7—9 points (APGAR score) at l—5minutes after birth, äs evidenced by the transient butmarked tachycardia and gradual slow-down in the neonatalheart rate patterns. Acute fetal distress in this case seemedto be caused by a rotation forceps Operation impeding thecirculation of the cord which was woUnd around theneck.


Takcmura, Qassification of perinatal dcpressions 27

mm. —*Fig. 4. A typical course of acute fetal disttess with primary, acute rcspiratory acidosis in the fetal capillaryblood within 5 minutcs just before dclivcry.

180-120-60-Jtzoi?-100-

0-

/77//7% -Fig. 5. Quite a typical case of subacute fetal distress with combined (respiratory äs well äs metabolic) acidosis reflect-ing the whole uterus ischemia induced by maternal hypotension and by tetanic uterine contractions. Note that suchmarked appearance of late FHR deceleration is to be called "bradycardia paradoxa" on the middle tracing.



2.2 Subacute fetal distress

The fetal oxygenation is also impeded by extra-amniotic, uteroplacental ischemia, which isusually caused by tetanic uterine contractions[7, 12] or by a decrease of systemic blood pressurein the mother [4, 16]. The hatched area infig. 3 (B) covers not only the fetus but the placentaand the Uterus.A typical case, such äs demonstrated in fig. 5, showedboth causes of insufficient fetal oxygenation. At first(top, left, third tracing), the maternal blood pressuredropped äs low äs 80 mmHg systolic; in addition,hypertonic, tachysystolic, tetanic contractions appeared toresult in prolonged moderate fetal bradycardia, whichwas normalized fairly quickly after correction of the hypo-tension and after the interval between the contractions hadbecome longer. After a while, in the late second stage oflabor, the recurrence of dystocic uterine contractions withätrpng bearing-down elevated the intrauterine pressuremarkedly and caused enhanced uterine ischemia, resultingin typical late FHR decelerations (UPI) called "bradycardiaparadoxa" [30], i. e., the FHR accelerates with contrac-tion and decelerates with relaxation. The l and 5 minuteAPGAR scores were 2 and 5, and pronounced fetalacidosis was present in the umbilical blood. The Pog andbase excess are both moderately lowered, so that acombined, respiratory äs well äs metabolic acidosiswas present in utero. Frequent and severe attacks of hy-poxia in the fetus and in the placenta and uterine musclesare probably the cause of this.

2.3 Chronic fetal distress

Another type of fetal distress, when the wholebody is depressed, can be induced by somecomplications in the mother. Severe cardio-pulmonary complications, such äs cyanotic heartdisorders, or heavy smoking are the cause ofmaldevelopment of the fetus [6], who might nothave sufficient oxygen reserves or tolerance towithstand the stress of vaginal delivery. Toxemiaof pregnancy is also a fairly dangerous com-plication for the mother äs well äs for the fetus.The high incidence of small-for-date babies intoxemic patients suggests that some nutritionaläs well äs metabolic disorders are present in thefetus and the placenta. Therefore, even withoutany predominant changes of the fetal heart rateor other cardio-vascular parameters, such a long-standing fetal or feto-maternal hypoxia may resultin chronic, primary metabolic acidosis of thefetus.

Fig. 6 describes a typical case of chronic fetal distress,followed by severe asphyxia i^onatorum with APGARscores l—4. Until the delivery no remarkable FHRchanges were noticed, but when we observed carefully,a very slight degree of late FHR deceleration was seenconsistently withevery contraction. The loss of irregularityof the beat-to-beat FHR variations was also found.Nevertheless the fetal capillary blood pH had beenastonishingly depressed (äs low äs 7.10 or lower) andcombined with a marked reduction of base excess from thebeginning. This is one of those rare cases in which therewas an enhanced metabolic acidosis in utero without änysign in the FHR except for the slight but quite consistentand insidious appearance of late FHR decelerations fromthe very early stages of labor.

3. Cybernetic view of the predominantpathogenesis of perinatal depressions(tab. 2)

As shown in fig. 3, these three types of fetaldistress correspond to their own spatial äs welläs frequency domains in the genesis of hypoxiain utero.Acute fetal distress means acute hypoxia andrespiratcry acidosis in the fetus due to the impair-ment of umbilical circulation. These conditionscan be induced and corrected within severalminutes.Subacute fetal distress due to recurrent blockadeof utero-placental circulation cannot kill the fetusso fast but it impairs the neonate if such a processlasts from a half to several hours during labor.Chronic and long-standing hypoxia with pri-mary metabolic acidosis in the fetus may involvea longer process of functional maternal blockade

1. Essential Depression (seconds):Neurogenic dysfunction in the onset of respiratoin

2. Acute Depression (minutes):Dysfunction of umbilical circulation

3. Subacute Depression (hours):Dysfunction of placental oxygenation

4. Chronic Depression (days):Metabolic dysfunction of the fetus/

5. Organic Depression (months):Dysfunction due to malformation and/or maldevelop-ment

Tab. 2. Classification of perinatal depressions accordingto the predominant pathogenesis with a particular dimen-sion in the spatial äs well äs in the frequency domains.



ro/n —*·

Fig. 6. One of the most typical cases o£ chtonic fetal distress complicated by toxemia o£ pregnancy. Note noparticular FHR variations until delivery except quite consistent appearances of slightest degree of late FHRdeceleration at every contraction. The fetus had primarily enhanced metabolic acidosis and became depressed withApgar score l—4 at one and five minutes after birth. Another finding of the FHR curves is complete loss ofbeat-to-beat irregularity.

and/or organic placental blockage of fetal oxy-genation and nourishment. An exposute of atleast several days is needed to so weaken thefetus that the stress of labor will cause irreparabledamage. But even with these three conditions nocomplete explanations can be given f or all of thepathogeneses of perinatal depressions. Withoutany signs of fetal acidosis or FHR variations, someinfants do not Start pulmonary respiration withina few seconds äs vigorously äs expected.Respiratory depressants such äs narcotics shouldbe taken into account in these cases of neurogenicdysfunction in the onset of respiration, socalled"essential depression".Others begin to show the Symptom of respiratorygrunting with some macroscopic malformationsor maldevelopment. These infants with anence-phaly, esophagotracheal fistula, diaphragm hernia-

rion or severe cardiac malformations, developedin the course of several months of pregnancy,cannot cry so actively äs normal babies; thisstate is called "organic depression".

4. A model of life in view of perinataldepressions

In any System the whole body is only controllableby an "across" variable, potential or pressure.The authority of a government can rule a nation.The supply and transport of electricity, city waterand fuel gas are all controlled by their respectivepressures and peripherally they are measured inquantity by the respective "through" variables,which are flows. The same is true for bloodcirculation so that blood pressute is one of themost important parameters in the body.

J. Perinat. Med. l (1973(


In fig. 7 we show a model of the circulation which webuilt for the Simulation study of heart rate control dyna-mics seen in respiratory sinus arrhythmia [23, 29]. Theinspiratory transient of heart rate acceleration may wellbe explained by the single loop of baroreceptic vagalcontrol of circulation, but the shifting of the level of thecontrolled variable, blood pressure, cannot be achievedwithout some contribution of parametric controls by thesympathicus, whose enhancement of cardiac contractilityand of peripheral vasoconstriction is indispensable but cannever be so prompt äs vagal control. The sympathetic loopis slower and longer in the frequency domain [35] and islarger in the spatial domain of its influence. It acts on thevagal control loop paramertically, forming a secondaryfeedback loop network. Thus a multiple loop controlSystem is established, at least for circulation dynamics.A living human body is much more complicated,with many Subsystems other than circulation,such äs the nervous, respiratory, digestive ormetabolic, and organic Systems. At birth aninfant should adapt all of these Systems to extra-uterine life, but impairments in any one of theSubsystems do not allow this. Essential depres-sion of the neonate is brought about within afew seconds after birth by the dysfunction ormaladaptation of the nervous System in the onsetof pulmonary respiration. Organic depression,

controlling System controlled system

Fig. 7. An example of multiple loop s control in thecirculatory System with parametric control mechanismsof higher sympathetic centers upon the rapidly responsive,vagal control of the heart.

particularly some life-threatening anomalies,cannot be caused in several hours but is the resultof months-long pregnancy.Considering the time dimension (in view ofhow fast the infant's life is established or destroyedat birth), we can now build a model of life (fig. 8)äs a multiple loops* feedback System with fiveSubsystems — nervous, circulatory, respirato-ry, metabolic and organic, each of whichcorresponds to our classification of perinataldepressions.The nervous System functions through theprompt transmission of electrical signals. Without

electricalphysical

physico-chemicalbio-chemical

bioiogical

Reproduction&

Development

Fig. 8. A mechanical, steady-state model of life, func-tioning äs a multiple loops' feedback control System witheach particular signal and" dimension in the frequency äswell äs spatial domain for the respective Subsystems. Thelower half suggests the biologically dynamic model oflife including the Subsystem of reproduction and develop-ment.

knowing anything about neural potentials and/orbrain waves, it is impossible to discuss how thebrain and the nervous System fünctiön.On the other hand, the most important parametersof circulation are physical variablem such äsblood pressure and flow, although they areclosely connected to the faster nervous System byan electrical signal, EGG, äs well äs to the slowerrespiratory system by physicochemicaL parameterssuch äs arterial blood Pco2-Respiration is controlled mostly by PacO2 phy-sicochemically [10] and is connected to the largerdigestive and metabolic system by the pH of thearterial blood.The organic system of a living body should bestudied for the shape (morphology), the repro-ductive ability (genetics) and for the interactionwith other molecules and organisms (pharmacol-ogy, immunology and bacteriology).


Takcmura, Classification of perinatal depressions 31

5. Comment

There has been some confusion about which isbetter äs a controlling parameter of childbirth,fetal pH or FHR patterns [l, 17, 28]. Now,however, according to the model and the classi-fication of perinatal disintegrating processes oflife, it is clear that the metabolic disorders in thefetus cannot be detected by only one of the cir-culatory parameters, natnely the fetal heart rate,and that the chemical parameters of the bloodsuch äs pH can never give äs quick detectionof the acutely depressed infant äs that providedby the FHR response [3, 21, 25]. As for perinataldepression, we have already well documented thefact that both early detection by the FHR andsure diagnosis by the pH together promise betterlabor monitoring [31]. The fetal heart rate isnot only a parameter of circulation but also ofplacental respiration in connection with theumbilical by-pass. But we must refrain from anover-evaluation of the FHR because the direct

Summary

Fetal monitoring during Jabor.and dynamic System analysisof the theoretical physiological basis have both made itpossible to build a model of fetal circulation which canexplain the mechanisms of fetal heart rate decelera-tions during uterine contractions and also make it possibleto classify perinatal depressions in five categories.Fetal circulation and respiration are not yet äs differen-tiated äs in the adult. So the System of fetal circulation andrespiration is modelled äs a simple parallel network,corporeal and placental, äs described in fig. 1. About halfof the fetal cardiac Output goes to the placenta via theumbilical circulation, which is a by-pass of the fetal corpo-real circulation. The very fast, baroreceptic controlSystem of the vagus and the rather slow, chemorecepticcontrol mechanism which is mainly due to thesympathicus are both described. According to theseassumptions, the cord type of variable FHR-decelera-tion is induced by activation of baroreceptors in the fetusdue to a sudden increase of hemodynamic impedance inthe umbilical circulation (fig. 2). The UPI or dip typeof late FHR deceleration is caused by chemoreceptorStimulation which in turn causes a sympathetic, gradualincrease of vascular impedance in the fetal corporealcirculation; this sacrifice of non-urgent tissües, such äsfetal skin, muscles and intestines, results in a slowingdown of the fetal heart rate and in a redistribution of theblood, mosdy to the heart and brain, thus conservingoxygen and energy consumption äs much äs possible.Therefore, whereas the former, reflex bradycardia, is aprimary self-defense mechanism activated by a prompt

measurement of pH teils us how placental oxy-genation is being carried out. On the other hand,the best time for FBA cannot be determinedwithout continuous monitoring of the FHRfrom the earliest possible stage of labor. FHRmonitoring in the late second stage of labor canprovide beat-to-beat Information so dynamicallythat the physician can avoid acute depression justbefore birth. But it is not entirely reliable sincea normal FHR may be recorded even in cases ofa severe metabolic acidosis which has endangeredthe fetus since the very early stages of labor.FHR monitoring and measurements of fetal bloodpH in the diagnosis of fetal acidosis can becompared to the smear test and the biopsy in thediagnosis of carcinoma of the uterine cervix.A diagnosis of all perinatal depressions can-not be made by considering only one of thefetal parameters during labor. It is better toknow the dynamic diagnostic spectrum of eachof the parameters well, and to use these para-meters accordingly.

single loop- feedback~in-a physical circulatory emergency,the latter, hypoxic bradycardia, is a secondary self-defense mechanism in hypoxic emergency with anotherslower chemical loop feedback activated in addition tothe former.So, in cases of such cord complications äs prolapse, trueknot, multiple loops, over-twisting, and too short or toolong and/or too thin a cord, the tight, protracted blockadeof umbilical circulation may induce "acute fetal distress"with the Symptoms of typical variable FHR decelerations,such äs marked prolonged fetal bradycardia of suddenonset, and with those of purely respiratory acidosis ofthe fetus, both of which can be quite reversible but yetmay kill the fetus in ten minutes or so, depending on thestate of the fetus (figs. 3 and 4).On the other hand, tetanic uterine contractions, maternalhypotension and physical or psychological excitementmay reduce the utero-placental blood flow, so thatischemia or hypoxia occurs, not only in the Uterus itself,but in the amniotic fluid, the placenta and the fetus, andmay induce combined fetal acidosis (respiratory äs welläs metabolic) together with the quite typical and pro-nounced appearance of late FHR decelerations. Theseare fairly reversible and are accompanied by markedrebound tachycardia between contractions, especially afteroxygen administration (fig. 5). The author calls this"subacute fetal distress99» because i t takes from a half toseveral hours for the development or the correction ofthis condition.

J. Petinat. Med. l (1973)


In addition, in cases of severe maiernal complications,such äs toxemia and catdio-pulmonary disorders,with or without organic changes of the placenta, "chronicfetal distress" frequently develops with signs of mild ormoderate late FHR decelerations on a slightly elevatedbaseline of diminished irregularity. These appear ratherinsidiously but consistently with every contraction fromthe early stages of labor and are accompanied by primarymetabolic acidosis of the fetus which is poorly reversible(fig- 6).Furthermore, regardless of the presence of intrauterineacidosis or bradycardia during labor, some neonates do notcry äs vigorously äs expected because of severe malforma-tions or serious birth injuries; these are the cause of"organic depression" in the perinatal period. Others,who develop apnea and perinatal depression with noobvious etiology, may be considered äs having"essential depression'* of the respiratory centers of the

fetus. This is mostly due to narcotic depressants of to vagalshock, which occurs within a ;few seconds after birth.In other words, according to how fast a fetus can bejeopardized, we now have a classification of perinataldepressions in five categories: essential, acute, subacute,chronic and organic. These are induced in seconds,minutes, hours, days, and months, respectively. More-over, every one of these corresponds to the dysfunctionof one of the multiple loop feedback control Systems oflife (figs. 7 and 8): the nervous, circulatory, respiratory,metabolic and organic Subsystems, each of which is tobe tested by their own specifie electrical, mechanical,physico-chemical, biochemical and biological parameters.Therefore, it is easy to understand that neither the fetalcapillary-blood pH nor the fetal heart rate alone cancover the entire diagnostic spectrum of perinataldepressions» because each feedback loop has a differentdynamic dimension in its deterioration and recovery withrespect to one of the five Subsystems of life.

Key words: Fetus, circulation, acid-base-balance, steady-state, deceleration, fetal distress, perinatal period, depres-' sion, cybernetics.

Zusammenfassung

Pathophysiologische Klassifizierung perinataler De-pressionen und kybernetische Aspekte in der Geburts-hilfe — eine Arbeitshypothese für Regelungs vor gangeim Bereich des Lebendigen.Anhand der Erfahrung mit hunderten von Feten, die wäh-rend der Geburt überwacht wurden und bei welchen dieMethode der dynamischen Systemanalyse angewandt wurde,konnte ein Modell des fetalen Kreislaufes entwickeltwerden, welches es ermöglicht, fetale Pulsdezelerationenwährend der Wehen zu erklären und mit dessen Hilfeperinatale Störungen in 5 pathophysiologische Kate-gorien eingeteilt werden können.Da Atmung und Kreislauf des Feten noch nicht so wiebeim Erwachsenen differenziert sind, kann der Kreislaufals parallelgeschaltetes System — Körper- und Plazentaskreislauf — betrachtet werden (Abb. 1). Etwa die Hälftedes fetalen Minutenvolumens wird zur Plazenta durchdie Nabelschnurgefäße geleitet; dies stellt eine Umgehungdes fetalen Körperkreislaufes dar.Die dynamische Systemanalyse erlaubt die Betrachtung derGeschwindigkeit, mit welcher das Pulsfrequenzkontroll-system bezüglich Frequenz und Phase reagiert. In diesemZusammenhang werden die Begriffe des schnellen Baro-rezeptorkontrollsystems (Vagus) und des langsamerenChemorezeptorsystems (Sympathicus) eingeführt. AufGrund dieser Annahmen würde der Nabelschnurtypus dervariablen FHF-Dezeleration durch die Aktivierungvon fetalen Barorezeptoren durch den plötzlichen An-stieg des hämodynamischen Widerstandes im Nabelschnur-kreislauf hervorgerufen (Abb. 2).Der „dip II" oder UPI-Typus (UPI = utero-plazentareInsuffizienz) der späten FHF-Dezeleration kann dann alsdurch Chemorezeptorstimulation bedingt erklärt wer-den, welche einen sympathischen, langsamen Anstieg vonGefäßwiderständen im fetalen Körperkreislauf hervorruft

unter Vernachlässigung weniger wichtiger Gewebe, wieHaut, Muskel oder Darm. Es ergibt sich dann eine Herz-schlagverlangsamung und Neuverteilung des Blutes indie zentralen Organe (Herz, Gehirn) und eine Spar-schaltung des gesamten Sauerstoff- und [Energie-verbrauches.Eine Reflexbradykardie ist also ein primärer Abwehr-reflex mit direkter Rückkopplung in einer Kreislauf-notsituation, während die Hypoxiebradykardie ein sekun-därer Abwehrmechanismus ist, in welchem die langsamere,chemische Rückkopplung zur ersteren hinzugefügt ist.Dementsprechend kommt es in Fällen von Nabelschnur-komplikationen (Vorfall, Knoten, Schlingen, Verdrehung,zu kurze, zu lange oder zu dünne Nabelschnur) zur anhal-tenden Blockierung der Nabelschhurdurchblutung und„akuten fetalen Störung" mit typischen variablen FHF-Dezelerationen und anhaltender Bradykardie des Fetensowie einer respiratorischen Azidose. Beide sind rever-sibel, können aber je nach dem Zustand des Feten innerhalbvon 10 Minuten zum Tode führen (Abb. 3, 4).Andererseits können tetanische Wehen, mütterliche Hypo-tension und physische oder psychische Aufregung dieDurchblutung des Uterus reduzieren, so daß Ischämieund Hypoxie von Fruchtwasser, Planzenta und Fet einekombinierte (respiratorische und metabolische) Azi-dose hervorruft, die mit typischen späten FHF-Dezelera-tionen einhergeht. Diese sind einigermaßen reversibel,da im Wehenintervall eine Tachykardie besteht, besondersnach Sauerstoffgabe (Abb. 5). Dieser Typ wurde„subakute fetale Störung" benannt, da das Leben desFeten erst nach einer halben Stunde oder einigen Stundenbedroht ist.Außerdem entwickelt sich häufig eine chronische fetaleStörung mit oder ohne organische Plazentaveränderungenbei ernsten mütterlichen Komplikationen wie Toxi-

J.Perinat.Med. l (1973)

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J. F. LEHMAN N S VERLAG M Ü N C H E N

(5)


kose oder Herz- und Lungenkrankheiten, wobei leichteoder mäßige späte FHF-Dezelerationen auf einer etwashöheren Basisfrequenz mit verminderten Schwankun-gen bestehen. Diese erscheinen langsam, jedoch ständigmit jeder Wehe vom Beginn der Wehentätigkeit an.Es besteht dabei hauptsächlich eine metabolische Azidosedes Feten, welche schwer zu beheben ist (Abb. 6).Weiterhin gibt es Neugeborene, welche, ohne daß einZusammenhang mit einer intrauterinen Azidose oderBradykardie besteht, weniger lebhaft als erwartet schreienund bei denen dann eine schwere Mißbildung festgestelltwird, wie z.1 B. Anencephalie, Zwerchfellhernie, Oesopha-gotrachealfistel, Herzfehler oder Hirnblutung. Bei ihnenwird eine „organische Depression*4 während der Peri-natalperiode angenommen. Wieder andere Neugeborenehaben eine Apnoe oder eine perinatale Depression ohneerkennbare Ursache; diese Depressionen werden als„essentielle Depression" des fetalen Atemzentrums durchNarkose oder Vagusschock angesehen; dies ereignet sichinnerhalb weniger Sekunden nach der Geburt. Demgemäß

ergibt sich aus den dynamischen Merkmalen des Zeit-raumes, in welchem der Fet bedroht ist, eine Klassifizie-rung der perinatalen Störungen in 5 Kategorien:essentiell, akut» subakut, chronisch und organisch,welche dementsprechend innerhalb von Sekunden, Minuten,Stunden, Tagen oder Monaten auftreten können unddementsprechned behandelt werden müssen. Jede ent-spricht einer Störung in einem der biologischen Mehr-fach-Rückkopplungssysteme (Abb. 7, 8), nämlich desNerven-, Kreislauf-, Atmungs-, Stoffwechsel- und organi-schen Subsystems. Diese müssen mit den ihnen entspre-chenden, spezifischen Signalen ausgewertet werden, näm-lich elektrischen, mechanischen, physikalisch-chemischen,biochemischen und biologischen Parametern. Es ist daherverständlich, daß weder das pH im fetalen Kapillar-blut noch die fetale Herzfrequenz allein das gesamtediagnostische Spektrum perinataler Depressionen um-fassen kann, da jeder Rückkopplungskreis eine anderedynamische Dimension bezüglich Verschlimmerung undErholung in einem der 5 Lebenssubsysteme hat.

Schlüsselworte: Fetus, Herzschlagregistrierung, Kybernetik,Dezeleration.

Säure-Basen-Haushalt, Perinatalperiode, Depression,

Resume

Classification physiopathologique des depressionsperinatales et cybernetique en Obstetrique — Unehypothese de travail pour un modele de vie.Les experiences de centaines de cas de surveillance foetalependant le travail, pour la pratique, et la methode dyna-mique d'analyse des bases physiologiques, pour la theorie,ont toutes deux conjointement permis d'elaborer unmodele de la circulation foetale qui peut expliquer lesmecanismes des decelerations du rythme cardiaquefoetal liees aux contractions uterines ainsi que declassifier les depressions perinatales en 5 categoriesselon le mecanisme physiopathologique par lequel un foetuspeut etre deprime a la naissance.La circulation et la respiration foetales ne sont pas aussidifferenciees que chez Fadulte pour avoir des systemesrespectifs distincts.Aussi, en ce qui concerne la fonction elle-meme, le Systemede la circulation et de la respiration foetale est organisecomme un simple reseau parallele, foetal et placentaire(fig. 1). Car, a peu pres la moitie du debit cardiaque foetalva au placenta par la circulation ombilicale qui court-circuite la circulation corporelle foetale.En vue d'une analyse d'un Systeme dynamique concernantla rapidite avec laquelle le rythme cardiaque contröle lesreponses de Forganisme en fr6quence et en phase, 2systemes doivent etre introduits: un, tres rapide, leSysteme de contröle baro-recepteur du vague efferent;un, plutöt lent, le mecanisme de contröle par leschemo-recepteurs, principalement du au sympathique.Selon ces presomptions, le type de ralentissement durythme cardiaque foetal par compression funiculaire estinduit par l'activation des baro-räcepteurs chez le

foetus, a un brusque accroissement de Pentravehemodynamique dans la circulation ombilicale (fig. 2).Le type «insuffisance utero-placentaire» ou dip II(decoleration tardive), est explique comme determine parla Stimulation des chemo-recepteurs qui entraine unaccroissement progressif, sympathique, des impedancesvasculaires dans la circulation corporelle foetale, sacri-fiant les tissus non urgents comme la peau, les muscleset les intestins du foetus pour obtenir le ralentissementdu rythme cardiaque foetal et la redistribution du sangprincipalement pour les organes centraux, coeur etcerveau, preservant la consommation d'oxygene et d'energieautant que possible dans sä totalite.Ainsi donc, tandis que le premier reflexe de bradycardieest un reflexe primaire d'autodefense, par un circuitrapide, unique de feedback physique dans Furgencecirculatoire, le tardif, la bradycardie hypoxique est unm£canisme secondaire d'autodefense dans Furgencehypoxique par un autre circuit de feedback chimiqueactive* plus lentement en adjonction au premier.Ainsi dans les cas de differentes complications du cordoncomme la procidence, un noeud vrai, des torsions circu-laires et briereto, le blocage serro prolongo de la circulationombilicale peut induire «la detresse foetale aigue» (fig. 3)avec comme marques, les symptomes de d€celerationsvariables typiques, une bradycardie foetale prolongeed'apparition soudaine ainsi qu'une acidose purementrespiratoire du foetus, chacune des deux pouvant etreentiarement reversibles mais cependant pouvant tuer lefoetus en 10 minutes ou plus, dependant de la part desouffrance chronique du foetus.

J. Perinat. Mcd. l (1973)

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D'un autre cote, des contractions utlrines tetaniques,une hypotension maternelle et une excitation physiqueou psychique peuvent reduire le flux sanguin utero-placentaire de teile sorte que Tischomie ou Phypoxie nonseulement dans Puterus lui-meme, mais encore dans leliquide amniotique, le placenta et le foetus, peut induireune acidose foetale combinee (respitatoire et motabo-lique) en association a des aspects tout ä fait typiqueset marques de decelerations tardives qui sont franchementreversibles de meme qu'accompagnes par des tebondsmarques de tachycardie entre les contractions, parti-culterement apres administration d'oxyg&ne. L'äuteurl'a appelee: «detresse foetale subaigue» parce qu'elle-demande environ une demie a quelques heures pour quela vie du foetus soit menacee ou soulagee de ce type•de detresse foetale.En outre, en cas de complications maternelles severes

• comme une toxemie et des desordres cardiopulmonairesavec ou sans modifications organiques du placenta,«la detresse foetale chronique» est frequemment

• developpee avec des signes de decelerations tardives durythme cardiaque foetal legeres ou moderees, sur une ligne

-de base legerement elevee, d'irregularite diminuee, quiapparait insidieusement mais de fagon consequente achaque contraction depuis le tout debut du travailaccompagnee par une acidose metaboüque foetaleprimaire, qu'est mediocrement reversibe.Par ailleurs, independamment de la presence de Pacidoseintra-uterine ou de la bradycardie pendant le travail, certainsnouveau-nes ne crient pas aussi vigoureusement queprevu, revelant qu'une malformation severe ou unelesion de naissance grave comme une anencephalie, une

hernie diaphragmatique, une fistule oesophagotrachoale,une anomalie cardiaque ou unethdmorragie corobrale pou-vait etre la cause de la «dopression organique» äleur periode porinatale. D'autres, qui developpent uneapnee et une depression porinatale, sans qu'on puissesuspecter de telles dtiologies, peuvent etre considore commeune «depression essentiell» des centres respiratoiresdu foetus, le plus souvent due ä des depresseurs narco-tiques ou un choc vagal survenu immediatement dans lesquelques secondes -de vie post-natale.Autrement dit, en fonction des caract6ristiques dynamiques,selon la rapidite avec laquelle un foetus peut etre menace,nous avons maintenant, une classification des depressionsperinatales en 5 categories qui sont: essentielle, aigue,subaigue, chronique et organique, lesquelles sontrespectivement induites ou traitees en secondes, minutes,heures, ans et mois.Bien plus, chacune d'entre eile correspond au dysfonction-nement de chacun des multiples circuits des systemes decontröle feedback de la vie, tels que les sous-systemesnerveux, circulatoire, respiratoire, metabolique etorganique qui doivent etre explores par leurs propressignaux spocifiques respectifs: electrique, mecanique,physicochimique, biochimique et biologique*Par consequent, il peut etre facile de comprendre que nile pH sanguin capillaire foetal, ni le rythme cardiaque foetal,ne peuvent isoloment recouvrir tout l'evential du spectrediagnostic des depressions perinatales de la vie, parce quechaque circuit de feedback a une dimension dynamiquedifFerente dans sä doterioration et son appartenance respec-tive a Tun des cinq sous-systemes de vie.

Mots-cles: Modele de circulation foetale, pathogenie de la detresse foetale, acidose foetale, decelerations du rythmecardiaque foetal, classification des depressions perinatales, cybernetique.

Acknowledgements

This investigation could not have been achieved without- sincere and long-standing encouragements of Prof. E. H.HON since the author worked at Yale in 1966—67 äsFulbright scholar particularly giving him an opportunity to

review all his datä of labör monitoring. The authordirects truthful thanks to Prof. IC. KURACHI of theDepartment and to Prof. E. J. QUILLIGAN of UniversitySouthern California for theif earnest guidances.

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Hikaru Takemura, M. D.Department of Obstetrics & GynecologyOsaka University Medical Schooll—2, Dojimahamadori 3-chomeFukushimaku, Osaka, Japan

J. Perinat. Med. l (1973) 3*

pathophysiological classification of perinatal depressions

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