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1. 1
Note - 1

2. Contents
Duration of Pregnancy
o Criteria for Establishment of Fetal Maturity
o Fetal pulmonary maturity
o Estimating Due Date
o Date of Onset of Labor
Physiology of Labor
o Terminology
o What Initiate Labor; Theories
o Fail-Safe Systems for Uterine Activation
o Maternal & Fetal compartment:
• Uterus; Placenta
o Four Phases of Parturition
2

3. Duration of Pregnancy
• The average duration of a normal human pregnancy is
– 267 days (38 weeks & 1 day), counted after conception, or
– 280 days (40 weeks) from the first day of the LNMP
• GA classification (ACOG and the Society for Maternal-Fetal Medicine (SMFM)
Preterm: < 37 weeks
• Remote From Term: 23 to 31 Weeks (In Ethiopia from 28 to 31 weeks)
• Early-preterm: from 310/7 to 34 weeks
• Late-preterm: 340/7 weeks through 366/7
Early term: 370/7 weeks through 386/7 weeks
Full term: 390/7 weeks through 406/7 weeks
Late term: 410/7 weeks through 416/7 weeks
Postterm ≥ 420/7 weeks (> 294 days → from the first day of the last menstrual period
(LMP)
3

4. Criteria for Establishment of Fetal Maturity
• Fetal maturity may be assumed if one of
the following criteria is met:
– Fetal heart tones have been documented as
present for
• ≥ 20 weeks by nonelectronic fetoscope or
• ≥ 30 weeks by Doppler ultrasound.
– 36 weeks since positive urine/serum
pregnancy test
– If the following supports a current GA of ≥
39 weeks
• CRL measured at 6 to 11 weeks
• Fundal height performed at 12 to 20 weeks
4
FD-HC-F
≥ 20 o Fetoscope
≥ 30 o Doppler
36 o HCG - Urine/serum
≥ 39 o CRL - at 6 to 11
o Fundal - at 12 to 20

5. Fetal Pulmonary Maturity
• If term gestation cannot be confirmed by two or more of the above obstetric clinical
or laboratory criteria, amniotic fluid analysis can be used to provide evidence of fetal
lung maturity
• The lung is the last vital organ of the fetus to mature to the extent necessary to
support extrauterine life
• RDS is associated with preterm birth due to insufficient production of pulmonary
surfactant.
– Pulmonary surfactant is synthesized by type II pneumocytes
– Surfactant consists of
• 90% phospholipids (primarily phosphatidylcholine and phosphatidylglycerol) and
• 10% proteins (surfactant proteins [SP]-A, SP-B, SP-C)
– Surfactant is packaged into lamellar bodies and is excreted into the alveolar space where it
unravels and forms a monolayer on alveolar surfaces. Lamellar bodies can also pass into the
amniotic cavity and, hence, are found in amniotic fluid
– Lamellar bodies (LB) are storage form of surfactant within type II pneumocytes
5

6. – The surfactant functions to reduce the surface tension in the
alveoli, preventing atelectasis
– When surfactant is deficient, the small alveoli collapse and the
large alveoli become overinflated and stiff, which has been
associated with increased risk of developing respiratory distress
– The status of fetal lung maturity is reflected in the concentration
of surfactant in the form of
• phospholipids and
• lamellar bodies - similar in size to platelets and can be quantified on a hematology
analyzer utilizing the platelet channel and used to estimate fetal lung maturity
6

7. 7
5 stages

8. • Pneumocyte
– surface epithelial cells of the alveoli
– Type I pneumocytes
• thin, squamous cells
• cover 95% of the internal surface of each alveolus
• ideal for gas exchange
– Type II pneumocytes
• larger, cuboidal cells
• are the progenitors of type 1 cells and are responsible for surfactant
production and homeostasis
8

9. • A variety of tests are available
• The parameters for evidence of fetal pulmonary maturity include:
1. Lecithin/sphingomyelin (L/S) ratio greater than 2.1
– Both are surfactants
– The major surface-active constituent of pulmonary surfactant is phosphatidylcholine (lecithin)
– As the fetus matures, the synthesis of lecithin increases, and by 34-36 weeks the amount of
lecithin present is sufficient to prevent alveolar collapse, but the amount of sphingomyelin
stays about the same
– L/S has been reported to be inadequate as a predictor of fetal surfactant maturity in many
complicated obstetric cases, particularly in patients with diabetes
– L/S ratios are also unreliable when the sample contains blood or meconium
• Meconium - can invalidate the final result.
• Blood - can decrease the result of the L/S ratio
9

10. 2. Presence of phosphatidylglycerol
o Phosphatidylglycerol (PG) is present only in amniotic fluid and respiratory tract effluent
o Presence – predict the absence of neonatal RDS with 99% probability
o Not affected with - blood or meconium
3. TDx-FLM assay (Fetal Lung Maturity II assay) shows ≥ 70 mg surfactant per gram of
albumin
o is a reagent system for the quantitative measurement of the ratio of surfactant to albumin in
amniotic fluid
o measures lung surfactants relative to albumin and the results are expressed as the
surfactant/albumin ratio
4. Presence of saturated phosphatidylcholine (SPC) ≥ 500 ng/mL in nondiabetic
patients (≥1000 ng/mL for pregestational diabetic patients)
o When phosphatidylglycerol was absent, phosphatidylcholine phosphorus was a reliable
predictor if measured 3 to 7 days before delivery
o The probability that respiratory distress syndrome would not occur was 94% when
phosphatidylcholine phosphorus was >6. When measurement was performed within 2 days of
delivery, the probability that respiratory distress syndrome would not occur fell to 69%
5. Lamellar body count exceeds 30,000/µL
– ≥ 50,000 (Gabbe 7th)
10

11. Estimating Due Date
• Due date (EDD) – definition
– 267 days (38 weeks & 1 day), counted after conception, or
– 280 days (40 weeks) from the first day of the LNMP
• Most accurate: 1st tm Us (Upto – 136/7 weeks)
– Ultrasound measurement of the embryo or fetus in the first trimester (up to and including 13 6/7 weeks of
gestation) is the most accurate method to establish or confirm gestational age (ACOG)
– CRL - more accurate
– Mean sac diameter measurements are not recommended for estimating the due date
– Beyond measurements of 84 mm (~140/7 weeks of gestation), accuracy of CRL to estimate gestational age
decreases
• If US after 220/7 weeks is used ➔ sub optimally dated (ACOG)
• In 2nd tm, BPD - accurately predicts gestational age
11

12. Calculating a Due Date
• 1st day of LNMP
• Naegele's rule: LMP – 2 month + 7 days
• Fundal height measurement
– accurate estimate of GA between 20 to 34 weeks.
– maternal bladder should be emptied prior to measurement.
– Maternal obesity may distort measurement accuracy
– Mayo Clinic Guide
• Measurement is generally defined as the distance in centimeters from the pubic bone to the
top of the uterus
• After 24 week, fundal height for a normally growing baby will match the number of weeks
of pregnancy ± 2 centimeters
• If pregnancy  assisted reproductive technology (ART)
– ART-derived gestational age should be used to assign EDD
– For instance, EDD for a pregnancy from IVF should be assigned using the age
of the embryo and the date of transfer
12

13. 13
Ultrasound is more accurate than LMP in dating

14. Date of Onset of Labor
• exact date of onset of labor - unpredictable
• Calculation based on Naegele’s formula can only give a rough
guide
– Naegale’s rule Rough estimate: spontaneous labor
• 4% at 40 weeks (EDD)
• 50% at 40 ±1week.
• 80% at 40 -2 & +1weeks.
• 10% at 42 weeks
• 4% at ≥43 weeks
14

15. Terminology
• A sequence of regular uterine
contractions that results in
• Progressive cervical effacement & dilatation
and
• involuntary bearing-down efforts,
– leading to expulsion of fetus (product of
conception) per vagina
• Clinical diagnosis: Triads
– regular painful uterine contractions
– progressive cervical E & D
– show (bloody discharge)
• is not synonymous with
labor
• the mode of expulsion
of the fetus and
placenta
• can take place without
labor as in elective
cesarean section
• may be vaginal, either
spontaneous or aided or
it may be abdominal
15
• the process of delivering the
fetus & placenta
– Parturient: a patient in labor
• Also called labor and delivery
• Physiological phases of
myometrial activty
– Phase 0: inhibitors active
– Phase 1: myometrial activation
– Phase 2: stimulatory phase
– Phase 3: involution

16. What Initiate Labor
• precise mechanism - still obscure
• Three general contemporaneous theories describe labor initiation
1) Functional loss of pregnancy maintenance factors
– no documented decrease in progesterone
– Rather, functional progesterone withdrawal
• ↓ in the concentration of progesterone receptors (PR)
• change in the ratio of PR isoforms A & B in both myometrium and membranes
2) Mature fetus is the source of the initial signal for parturition commencement
– Placental production of CRH near term activates the fetal hypothalamic-pituitary axis
and results in increased production of dehydroepiandrostenedione by the fetal adrenal
gland
3) Synthesis of factors that induce parturition
– Fetal dehydroepiandrostenedione is converted in the placenta to estradiol and estriol.
– Placenta-derived estriol potentiates uterine activity by enhancing the transcription of
maternal (likely decidual) - PGF2α, PG receptors, oxytocin receptors, and gap-junction
proteins
16

17. • Fetus has a central role in the initiation of term labor in nonhuman mammals
– in humans, the fetal role is not completely understood
In sheep
• term labor is initiated through activation of the fetal hypothalamic-pituitary adrenal
(HPA) axis, with a resultant increase in fetal ACTH and cortisol
• Fetal cortisol
o increases production of estradiol
o decreases production of progesterone by a shift in placental metabolism of cortisol dependent on
placental 17α-hydroxylase
– These change stimulates placental production of oxytocin and PG, particularly PGF2α,
which in turn promotes myometrial contractility
– If this increase in fetal ACTH and cortisol is blocked, progesterone levels remain
unchanged, and parturition is delayed
• In contrast, humans lack placental 17α-hydroxylase,
– maternal and fetal levels of progesterone remain elevated, and
– no trigger exists for parturition because of an increase in fetal cortisol near term
• Most species have distinct diurnal patterns of contractions and delivery, and in
humans, the majority of contractions occur at night
17

18. 18
Fetal Role Placental Role Maternal Role
 Hypothalamus – CRH (CRH
also come from placental
production)
 Anterior Pituitary – ACTH
 Adrenal – Cortisol & DHEAS
 Fetuses with adrenal
hypoplasia – usually post
date
 Produces CRH which induces fetal pituitary to
produce ACTH
 Induced by fetal cortisol, it ↑es oxytocin, PG,
E, interleukin (1, 6 & 8)
 Induced by fetal DHEAS, it ↑es estrogen
 Fetal cortisol ↓es progesterone production &
this ↑es uterine sensitivity to stretching
 Oxytocin is normally produced in the
hypothalamus and released by
posterior pituitary
 ↑es myometrial receptors for PG,
oxytocin,
 ↑es Gap junction
 ↑es decidual PGF2a
 Stretch receptors (No & sensitivity)
Pro pregnancy: Progesterone, Prostacyclin (PGI-2), Relaxin, Parathyroid hormone-
related peptide, Nitric oxide, Calcitonin gene-related peptide, Adrenomedullin,
Vasoactive intestinal peptide
Prolabor factors: Estrogen, Oxytocin, Prostaglandins, Prostaglandin dehydrogenase,
Inflammatory mediators

19. Theory Proposed mechanism
Hormonal
Estrogen theory
 Estradiol raises myometrial oxytocin receptor concentrations - increases contractibility
 Estrogen ↑es excitability of the myometrium and prostaglandins synthesis
Progesterone withdrawal
theory
 Progesterone: enhance oxytocin receptor degradation and inhibit oxytocin activation of its receptor at
the cell surface
 Classical progesterone withdrawal does not cause human parturition
 in humans the inhibition of progesterone action is important for activation phase of parturition
• Through Changes in the relative expression of the progesterone receptor
Prostaglandins theory  PG E2 and F2α are powerful stimulators of uterine muscle activity
Oxytocin theory
 powerful stimulator of uterine contraction
 Near term: secretion of oxytocinase enzyme from placenta is decreased due to placental ischaemia
Fetal cortisol theory
 CRH from fetal placenta and hypothalamus - promote myometrial quiescence during most of
pregnancy and aids myometrial contractions with onset of parturition
o Early pregnancy: with its CRHR1 receptor activates the Gs-adenylate cyclase-cAMP signaling pathway
→ inhibition of inositol triphosphate (IP3) and stabilization of (Ca2+)i levels
o Term:activation of G proteins Gq and Gi → stimulation of IP3 production → increase [Ca2+] which
increases uterine contractility
Mechanical
Uterine distension theory  This explains the preterm labor in case of multiple pregnancy and polyhydramnios
Mechano transduction
 Stretch of the lower uterine segment by the presenting part near term ↑es expression of gap
junction protein, connexin 43, as well as oxytocin receptors
19
Theories

20. Prostaglandins Role
• Prostaglandins interact with a family of eight different G-
protein– coupled receptors, several of which are
expressed in myometrium and cervix
• Prostaglandins are produced using plasma membrane-
derived arachidonic acid, which usually is released by the
action of phospholipase A2 or C
• Arachidonic acid can then act as substrate for both type 1
and 2 prostaglandin H synthase (PGHS-1 and -2), which are
also called cyclooxygenase-1 and -2 (COX-1 and -2)
• Both PGHS isoforms convert arachidonic acid to the
unstable prostaglandin G2 and then to prostaglandin H2
• Amnion - major source for amnionic fluid prostaglandins
• Prostaglandin transport from the amnion through the
chorion to access maternal tissues is limited by expression of
PGDH
• 15-hydroxyprostaglandin dehydrogenase (PGDH)
– inactivate prostaglandins
– So determine - myometrial responses to prostaglandins
• Because it balances prostaglandin synthesis versus metabolism
20
Tocolytic actions of specific NSAIDs

21. The most important differences
between the two isoforms
• COX-1
– expressed in most tissues, but variably
– a "housekeeping" enzyme, regulating
normal cellular processes (such as
gastric cytoprotection, vascular
homeostasis, platelet aggregation, and
kidney function), and it is stimulated
by hormones or growth factors
• COX-2
– constitutively expressed in the brain,
in the kidney, in bone, and probably in
the female reproductive system
21

22. Fail-Safe Systems for Uterine Activation
• a "parturition cascade“ removes the mechanisms
maintaining uterine quiescence and recruits factors
promoting uterine activity
– labor results from a down-regulation of pathways that favor
uterine quiescence leading to a relative dominance of
stimulatory pathways that increase intracellular calcium
bioavailability and promote myometrial contractility
22

23. Uterus
Myometrial layer - composed of smooth muscle cells
• In contrast to striated muscles (skeletal or cardiac)
– smooth muscle cell is not terminally differentiated
❑ So readily adaptable to environmental changes
❑ Varied stimuli such as mechanical stretch, inflammation, and endocrine and paracrine
signals can modulate the transition of the smooth muscle cell among phenotypes that
provide cell growth, proliferation, secretion, and contractility
• Additional qualities of smooth muscle
o greater degree of shortening with contractions than striated muscle cells
o forces can be exerted in any direction
o smooth muscle fibers are organized in long, random bundles throughout the cells →
greater shortening and force-generating capacity
❑ Greater multidirectional force generation in the uterine fundus compared with that of
the lower uterine segment enables to bear irrespective of lie / presentation of fetus
23

24. 24
Physical structure of smooth muscle
Structure of a Skeletal Muscle Fiber

25. • During pregnancy, cervix has multiple functions that include:
– (1) maintenance of barrier function to protect the reproductive tract from
infection,
– (2) maintenance of cervical competence despite greater gravitational
forces as the fetus grows, and
– (3) orchestration of extracellular matrix changes that allow progressively
greater tissue compliance.
• In nonpregnant women, the cervix is closed and firm, and its
consistency is similar to nasal cartilage
– By the end of pregnancy, the cervix is easily distensible, and its
consistency is similar to the lips of the oral cavity
25

26. Placenta
26
Amnion
• synthesizes prostaglandins
• late in pregnancy, synthesis is augmented by increased phospholipase A2 and prostaglandin H
synthase, type 2 (PGHS-2) activity
• avascular tissue: resistant to penetration by leukocytes, microorganisms, and neoplastic cells
– also - selective filter to prevent fetal particulate-bound and skin secretions from reaching the maternal
compartment
– In this manner, maternal tissues are protected from amnionic fluid constituents that could prematurely
accelerate decidual or myometrial activation or could promote adverse events such as amnionic fluid
embolism

27. Chorion
• is a primarily protective tissue layer and provides immunological acceptance
• It is also enriched with enzymes that inactivate uterotonins, which are agents that stimulate
contractions
• During pregnancy, the transport of prostaglandins from the amnion to maternal tissues is
limited by expression of the inactivating enzymes, prostaglandin dehydrogenase (PGDH),
in the chorion
– During labor, PGDH levels decline, and amnion-derived prostaglandins can influence membrane
rupture and uterine contractility
– Inactivating enzymes include prostaglandin dehydrogenase, oxytocinase, and enkephalinase
Decidua
• at the end of pregnancy, decidua induce inflammatory signals and withdraw active
immunosuppression, which contribute to parturition initiation
• The role of decidual activation in parturition is unclear but may involve local
progesterone metabolism and higher prostaglandin receptor concentrations, thus
enhancing uterine prostaglandin actions and cytokine production.
27

28. Four phases of parturition
28
• When parturition is abnormal, then preterm labor,
dystocia, or postterm pregnancy may result
• Parturition can be arbitrarily divided into four overlapping
phases that correspond to the major physiological transitions
of the myometrium and cervix during pregnancy
Uptodate, Gabbe
▪ Phase 0: inhibitors active
▪ Phase 1: myometrial activation
▪ Phase 2: stimulatory phase
▪ Phase 3: involution
William
▪ Phase 1: inhibitors active
▪ Phase 2: myometrial activation
▪ Phase 3: stimulatory phase
▪ Phase 4: involution

29. 29

30. 30

31. Phase I
comprises 95 percent of pregnancy
myometrial cells - noncontractile state & uterine muscle - unresponsive ➔
Myometrial Relaxation
low-intensity myometrial contractions (Braxton Hicks contractions) may be felt
Accelerated Uterotonin Degradation: PGDH (prostaglandins), enkephalinase
(endothelins); oxytocinase (oxytocin); diamine oxidase (histamine); catechol O-
methyltransferase (catecholamines); angiotensinases (angiotensin-II); platelet-
activating factor – PAF (PAF acetylhydrolase)
Decidua – suppressed synthesis of prostaglandins, particularly PGF2α
Cervical Softening  increased vascularity, cellular hypertrophy and hyperplasia,
and slow, progressive compositional and structural changes in the extracellular
matrix
31

32. Phase II
 readies the uterus for the subsequent stimulation phase
 Functional Progesterone Withdrawal (not decreased secretion)
– progesterone inactivation
– myometrium and cervix become refractory to progesterone’s inhibitory actions
 Myometrial Changes:
– Rise in CAPs, myometrial oxytocin receptors and gap junction proteins, such as connexin-43, markedly rise in
number
– formation of the lower uterine segment from the isthmus
 Cervical Ripening
– transition from the softening to the ripening phase begins weeks or days before labor
Cervix composition
– Nonpregnant: 50% sm/mu - at the internal os but only 10% at the external os
– Pregnant: high ratio of fibroblasts to smooth muscle cells, and extracellular matrix contributes significantly to
overall tissue mass
32

33. 33
Phase 1: fibril size is uniform and fibrils are well organized, although a
decline in cross-link density aids softening
Phase 2: fibril size is less uniform, and spacing between collagen fibrils and fibers is greater and disorganized

34.  Fetal Contributions to Parturition
 Uterine Stretch (mechano transduction): Induces CAPs & increases expression of connexin-43 and
oxytocin receptors
 Fetal Endocrine
– fetal hypothalamic pituitary-adrenal-placental axis
– Placental–fetal adrenal endocrine cascade
• placental CRH stimulates fetal adrenal production of dehydroepiandrosterone sulfate (DHEA-S)
and cortisol
• Fetal cortisol stimulates production of placental CRH, which leads to a feed-forward cascade
that enhances adrenal steroid hormone production
• unlike hypothalamic CRH, which is under glucocorticoid negative feedback, cortisol instead
stimulates placental CRH production
– This ability makes it possible to create a feed-forward endocrine cascade that does not end
until delivery
– CRH acts to augment myometrial contractile force in response to PGF2α
– CRH stimulates fetal adrenal C19-steroid synthesis, thereby increasing substrate for placental
aromatization
– Some have proposed that the rising CRH level at the end of gestation reflects a fetal-placental clock
34

35.  Fetal lung products:
– Surfactant protein A (SP-A) - activates myometrial contractility
– Platelet-Activating Factor - uterotonic agent
 Fetal-Membrane Senescence
–  stretch and oxidative stress
– propagates inflammatory signals that further weaken the fetal membrane and activate signals in
the decidua and myometrium to initiate parturition
Fetal Anomalies and Delayed Parturition
• Inherited placental sulfatase deficiency
– pregnancies with markedly diminished estrogen production may be associated with prolonged
gestation
• fetal anencephaly with adrenal hypoplasia
– anomalous fetal brain-pituitary-adrenal function – delayed labor
• brain anomalies of fetal calf, fetal lamb, and sometimes the human fetus delay the normal timing of
parturition
• fetal abnormalities that prevent or severely reduce the entry of fetal urine or lung secretions into
amnionic fluid do not prolong human pregnancy
– Examples are renal agenesis and pulmonary hypoplasia, respectively
– Thus, a fetal signal through the paracrine arm of the fetal–maternal communication system does
not appear to be mandated for parturition initiation
35

36. Phase III
 synonymous with active labor, which is customarily divided into three stages
 “Show” or “bloody show
– extrusion of the mucus plug that had previously filled the cervical canal during pregnancy
– Shows that labor is already in progress or likely will ensue in hours to days
 Unique among physiological muscular contractions, those of uterine smooth muscle during labor are
painful. Several possible causes have been suggested
– (1) Hypoxia of the contracted myometrium—such as that with angina pectoris;
– (2) Compression of nerve ganglia in the cervix and lower uterus by contracted interlocking muscle bundles;
• Uterine contractions are involuntary and, for the most part, independent of extrauterine control
• Neural blockade from epidural analgesia does not diminish their frequency or intensity
• In other examples, myometrial contractions in paraplegic women and in women after bilateral lumbar sympathectomy are normal
but painless
– (3) Cervical stretching during dilation
– (4) Stretching of the peritoneum overlying the fundus
 Ferguson reflex
– A phenomenon in which mechanical stretching of the cervix enhances uterine activity
– exact mechanism is unclear, and release of oxytocin has been suggested but not proven
– Manipulation of the cervix and “stripping” the fetal membranes is associated with a rise in blood levels of
prostaglandin F2α metabolites
36

37. Sequence of development of LUS & rings in the uterus at term and in labor
• The passive lower uterine segment is derived from isthmus
• upper segment contracts, retracts, and expels the fetus
• the softened lower uterine segment and cervix dilate and thereby form a greatly expanded, thinned-
out tube through which the fetus can pass
• if the entire myometrium, including the lower uterine segment and cervix, were to contract simultaneously and
with equal intensity, the net expulsive force would markedly decline
• Physiological retraction ring
– boundary between lower segment thinning and concomitant upper segment thickening
• Pathological retraction ring
– When the thinning of the lower uterine segment is extreme, as in obstructed labor, the ring is prominent and forms a
pathological retraction ring
– develops from the physiological ring
– This abnormal condition is also known as the Bandl ring
37
Anat. I.O. = anatomical internal os;
E.O. = external os;
Hist. I.O. = histological internal os;
Ph.R.R. = physiological retraction ring

38. • Ancillary Forces
– Maternal intraabdominal pressure
• Cervical Changes
– two fundamental changes - occur in the ripened cervix
– Effacement: shortening of the cervical canal from a length of approximately 3
cm to a mere circular orifice with almost paper-thin edges
– Dilation
• The process of cervical effacement and dilation causes formation of the
forebag of amnionic fluid
– Early rupture of the membranes does not retard cervical dilation so long as the
presenting fetal part is positioned to exert pressure against the cervix and lower
segment
38

39.  First Stage: Clinical Onset of Labor
– Latent phase
– Active phase: subdivided further into
• Acceleration phase
• Phase of maximum slope, and
• Deceleration phase
 Second Stage: Fetal Descent
– Pelvic Floor Changes
 Third Stage: Delivery of Placenta and
Membranes
– Cleavage of placenta is aided greatly by the
loose structure of the spongy decidua
– hematoma is the result rather than the cause
of the separation
Mzm of separation
– Schultze mechanism: blood from the
placental site pours into the membrane sac
and does not escape externally until after
extrusion of the placenta
– Duncan mechanism: placenta separates first
at the periphery and blood collects
between the membranes and the uterine
wall and escapes from the vagina
• In this circumstance, the placenta descends
sideways, and its maternal surface appears first 39
On the basis of expected evolution of the dilatation and
descent curves into three functional divisions
▪ Preparatory division: latent & acceleration phases
▪ Dilatational division: phase of maximum slope of dilatation
▪ Pelvic division: deceleration phase & second stage, which
is concurrent with the phase of maximum slope of fetal
descent

40. Uterotonics
• Prostaglandin F2α and oxytocin bind
their respective receptors during labor
to open ligand-activated calcium
channels ➔ releases of calcium from
the sarcoplasmic reticulum ➔
Depolarization
Oxytocin
• a peptide hormone synthesized in the
hypothalamus and released from the
posterior pituitary
• potent uterotonic agent at IV infusion
rates of 1 to 2 mIU/min
• Oxytocin is inactivated largely in the
liver and kidney
– during pregnancy, it is degraded
primarily by placental oxytocinase
• Its biologic half-life is approximately 3
to 4 minutes,
– but it appears to be shorter when higher
doses are infused
• Oxytocin - dual role in parturition
– directly stimulates uterine contractions
– Indirectly stimulate amnion and decidua
to produce PG
• These pathways (of PGF2α and intracellular
calcium) have been the target of multiple
tocolytic agents: indomethacin, calcium
channel blockers, β-mimetics (through
stimulation of cAMP), and magnesium
Prostaglandins
• Role
– in phase 2 : less well defined
– critical role: in phase 3
Endothelin-1
• ↑es intracellular ca in smooth muscle
40

41. Phase IV – Puerperium
• Uterine involution
– occurs after delivery and is mediated primarily by oxytocin
• Complete uterine involution: 4-6 wks
• Infertility persist as long as breast feeding is continued (lactation → anovulation &
amenorrhea)
• Immediately and for about an hour after delivery, the myometrium remains persistently
contracted. This directly compresses large uterine vessels and allows thrombosis of their
lumens to prevent hemorrhage. This is typically augmented by endogenous and
pharmacological uterotonic agents
• Uterine involution and cervical repair are prompt remodeling processes that restore these
organs to the nonpregnant state.
• These protect the reproductive tract from invasion by commensal microorganisms and
restore endometrial responsiveness to normal hormonal cyclicity
41

42. • During the early puerperium, lactogenesis and milk let-down
begin in mammary glands
– Reinstitution of ovulation signals preparation for the next
pregnancy
– Ovulation generally occurs within 4 to 6 weeks after birth
• However, it is dependent on the duration of breastfeeding and
lactation-induced, prolactin-mediated anovulation and
amenorrhea
42