Book reading

PHYSIOLOGY OF
LABOR
Presenter: dr. Muthia Puspasari
Moderator: Dr. dr. Nuswil Bernolian, Sp.O.G, Subsp. K.Fm, MARS

RESIDENCY PROGRAM OF OBSTETRICS AND GYNECOLOGY

FACULTY OF MEDICINE SRIWIJAYA UNIVERSITY
DR. MOHAMMAD HOESIN HOSPITAL PALEMBANG
 OUTLINE

1 Maternal and Fetal 5 Phase 2: Preparation for

Compartments Labor

2 Sex Steroid Hormone Role

6 Phase 3: Labor

3 Prostaglandins Role
7 Uterotonins in Parturition
Phase 3

4 Phase 1: Uterine 8 Phase 4: The Puerperium

Quiescence & Cervical
Softening
MATERNAL AND FETAL
COMPARTMENTS
UTERUS AND CERVIX

Myometrial layer  composed of bundles of smooth muscles

Advantages of smooth muscles:

The degree of smooth muscle cell shortening

Forces can be exerted in smooth muscle cells
with contractions may greater than striated
in multiple directions
muscle cells.

The plexiform arrangement  aids Greater multidirectional force generation in

augmented shortening and force-generating the uterine fundus  optimize expulsive
capacity force vectors.
ENDOMETRIUM

Endometrium is transformed by pregnancy hormones

and is then termed decidua.

Composed of stromal cells and maternal immune cells, the decidua

serves to maintain the pregnancy via unique immunoregulatory
functions that suppress inflammatory signals during gestation.
 UTERUS AND CERVIX

Maintaining the epithelial barrier

 protect the reproductive tract Cervix:
infection • By the end of pregnancy  easily
distensible

Function of Sustaining cervical competence • Has a high ratio of fibroblasts to

cervix as the fetus grows smooth muscle cells

• Smooth muscle cells: 50% of stromal

cells at the internal os, 10% at the
Orchestrating extracellular matrix external os.
(ECM) changes  greater tissue
compliance.
PLACENTA

The fetal membranes 

amnion and chorion

AMNION CHORION
• Provides the fetal membranes’ tensile strength • Protective tissue layer and provides
 resist membrane tearing and rupture immunological acceptance
• Highly resistant avascular tissue to • Enriched with enzymes that inactivate
penetration by leukocytes, microorganisms, uterotonins
and neoplastic cells • Inactivating enzymes such as prostaglandin
• Selective filter  prevent fetal particulate dehydrogenase, oxytocinase, and
from reaching the maternal compartment. enkephalinase
SEX STEROID HORMONE ROLE
SEX STEROID HORMONE ROLE

Estrogen and progesterone  components of a molecular system that maintains uterine

quiescence

• Progesterone inhibits the events leading to parturition

PROGESTERON
• The removal of progesterone, that is, progesterone withdrawal,
E directly precedes progression of parturition.

ESTROGEN • At the end of pregnancy  mediate uterine activation and cervical ripening

Estrogen:
NUCLEAR Progesterone:
Estrogen receptor α (ERα) and
RECEPTOR PR-A and PR-B
estrogen receptor β (ERβ)
PROSTAGLANDINS ROLE
PROSTAGLANDIS ROLE

Prostaglandins are lipid molecules with hormone-like actions play prominent role 
myometrial contractility, relaxation, and inflammation.

Prostaglandins interact with a family of eight different G protein–

coupled receptors

The amnion synthesizes several bioactive peptides and prostaglandins that

cause myometrial relaxation or contraction

The amnion is likely the major source for amnionic fluid prostaglandins, in
addition to the myometrium
Figure 2. Overview of the prostaglandin biosynthetic pathway. PG = prostaglandin; PGDH =
prostaglandin dehydrogenase; PGE2 = prostaglandin E2; PGF2α = prostaglandin F2α; PGH2 =
prostaglandin H2; PGHS = prostaglandin H synthase; PGI2 = prostaglandin I2; PLA2 = phospholipase
A2; PLC = phospholipase C.
PHASE 1: UTERINE QUIESCENCE
AND
CERVICAL SOFTENING
THE PHASES OF PARTURITION
Figure 3. Labor course divided on the
basis of expected evolution of the
dilatation and descent curves into three
functional divisions.
 THE QUIESCENCE OF PHASE
1
MYOMETRIAL RELAXATION & CONTRACTION

Quiescence Contractility

Diminished intracellular crosstalk and reduced Enhanced interactions between the actin and
intracellular Ca2+ levels, myosin proteins,

Ion-channel regulation of cell membrane Heightened excitability of individual

potential myometrial cells

Activation of the stress–unfolded protein Promotion of intracellular crosstalk 

response by the uterine endoplasmic reticulum synchronous contractions to develop.

Uterotonin degradation
Figure 5. Uterine myocyte relaxation and contraction. A. Uterine relaxation is maintained by factors that increase
myocyte cyclic adenosine monophosphate (cAMP) levels. B. Uterine contractions result from reversal of these
sequences.
 • Suppression of prostaglandin production here persists
DECIDUA throughout most of pregnancy, and suppression
withdrawal is a prerequisite for parturition

CERVICAL • The initial stage of cervical remodeling

SOFTENING (softening) begins in phase 1 of parturition

CERVICAL • Matrix changes, collagen undergoes

CONNECTIVE conformational changes that alter tissue
TISSUE stiffness and flexibility
PHASE 2: PREPARATION FOR
LABOR
 • Changes in progesterone-receptor (PR)
Progesterone • Local progesterone inactivation by steroid -
Withdrawal metabolizing enzymes

Myometrial • Formation of the lower uterine segment from

Changes the isthmus

• Matrix disorganization
Cervical Ripening • Inflammatory changes

Fetal Contribution to • Uterine Strecth

Parturition • Fetal Endocrine Cascades
Figure 9. The placental–fetal adrenal endocrine cascade. In late gestation, placental corticotropin-releasing hormone
(CRH) stimulates fetal adrenal production of dehydroepiandrosterone sulfate (DHEA-S) and cortisol. The latter
stimulates production of placental CRH, which leads to a feed-forward cascade that enhances adrenal steroid hormone
production.
PHASE 3: LABOR
PHASE 3: LABOR

The stage of the stage of

cervical The stage of fetal placental
effacement and expulsion separation and
dilation expulsion
FIRST STAGE: CLINICAL ONSET OF LABOR
Uterine Labor Contractions
• Bloody show
• Painful uterine contraction
• Active phase labor, the duration of each
contraction: 30-90 seconds and averages 1
minute
Distinct Lower and Upper
Uterine Segments
• The upper segment is firm during
contractions, the lower segment is softer,
distended, and more passive.
• Lower segment thinning and concomitant
upper segment thickening  a boundary
between the two is marked by a ridge on
the inner uterine surface (the physiological
retraction ring.
Figure 10. Sequence of development of the segments and rings in the uterus at term and in labor. Note comparison between the
nonpregnant uterus, the uterus at term, and the uterus during labor. The passive lower uterine segment is derived from the isthmus, and
the physiological retraction ring develops at the junction of the upper and lower uterine segments. The pathological retraction ring
develops from the physiological ring
Figure 11. The uterus at the time of vaginal
delivery. The active upper segment retracts
around the presenting part as the fetus
descends through the birth canal. In the
passive lower segment, there is considerably
less myometrial tone
FIRST STAGE: CLINICAL ONSET OF LABOR

Changes in Uterine
Ancillary Forces Cervical Changes
Shape
• Each contraction Contraction of the • Effacement and dilation
gradually elongates the abdominal muscles and occur in the ripened
ovoid uterine shape (5- forced respiratory efforts cervix  fully dilate to
10 cm and narrows the with the glottis closed  a diameter of 10 cm
horizontal diameter. pushing • cervical dilation is
• The lower segment and divided into latent and
cervix are flexible  active phases
pulled upward and
around the lower pole of
the fetus
Figure 12. Schematic showing effacement and
dilation. A. Before labor, the primigravid cervix is
long and undilated in contrast to that of the
multipara, which has dilation of the internal and
external os. B. As effacement begins, the multiparous
cervix shows more dilation and funneling of the
internal os compared with the primigravid cervix. C.
As complete effacement is achieved in the
primigravid cervix, dilation is minimal. The reverse
is true in the multipara.
Figure 13. Hydrostatic action of membranes in effecting cervical effacement and dilation. With labor progression, note the
changing relations of the internal and external os in (A), (B), and (C). Although not shown in this diagram, with membrane
rupture, the presenting part, applied to the cervix and the forming lower uterine segment, acts similarly.
SECOND STAGE: FETAL DESCENT

• Many nulliparas  engagement of the head is accomplished before labor begins.

• In normal labor  a typical hyperbolic curve is formed when the station of the fetal
head is plotted

• During second-stage labor  the speed of descent is maximal and is maintained until the
presenting part reaches the perineal floor

• In nulliparas, the presenting part typically descends slowly and steadily.

• In multiparas, descent may be rapid.

PELVIC FLOOR CHANGES

• The important component of the floor  levator ani muscle and the fibromuscular
connective tissue that covers its upper and lower surfaces

• The most marked change: stretching levator ani muscle and thinning of the central
portion of the perineum (almost transparent membranous structure less than 1 cm thick)

• When the perineum is distended maximally, the anus becomes markedly dilated and
presents an opening (2 to 3 cm in diameter) and through which the anterior wall of the
rectum bulges.
THIRD STAGE: DELIVERY OF PLACENTA AND MEMBRANES

• This stage begins immediately after fetal delivery and involves separation and expulsion of the
placenta and membranes

• This sudden diminution in uterine size is inevitably accompanied by a decrease in the area of the
placental implantation site

• Cleavage of the placenta is aided greatly by the loose structure of the spongy decidua

• Membranes usually remain in situ until placental separation is nearly completed  peeled of the
uterine wall, partly by further myometrium contraction and partly by traction that is exerted by the
separated placenta as it descends during expulsion.

• Completion of the third stage  alternately compressing and elevating the fundus, while exerting
minimal traction on the umbilical cord
Figure 14. Diminution in size of the
placental site after birth of the newborn. A.
Spatial relations before birth. B. Placental
spatial relations after birth.
Figure 15. Postpartum, membranes are
thrown up into folds as the uterine cavity
decreases in size.
UTEROTONINS IN PARTURITION
PHASE 3
UTEROTONINS IN PARTURITION
PHASE 3

Oxytocin
• Strikingly rising in myometrial and decidual tissues near the end of gestation

• Acting on decidual tissue  promote prostaglandin release

• Synthesis directly in decidual and extraembryonic fetal tissues and in the placenta

• Maternal serum oxytocin levels are elevated: during phase 3 of parturition, early
puerperium, and breastfeeding
UTEROTONINS IN PARTURITION
PHASE 3
Prostaglandin fetal membranes &
placenta produce
prostaglandins
• Levels of prostaglandins increased during labor

• Receptor PGE2 and PGFα are expressed in uterus

follow an
and cervix weakening fetal
inflammatory
membranes
response
• Treatment with prostaglandin  abortion or labor
at any gestational age
together rise in
• Prostaglandin production in myometrial 
cytokine and degrade the ECM
efficient of activating contractions prostaglandin
UTEROTONINS IN PARTURITION
PHASE 3
• Family of 21-amino-acid peptides  induce myometrial
contraction
ENDHOTELIN • Produced in the myometrium of term gestations and induce
1 synthesis of other contractile factors (prostaglandins and
inflammatory mediators)

• A potent vasoconstrictor  modulation of uteroplacental

blood flow
ANGIOTENSI • Normotensive pregnancy: AT2R  lead to vasodilation (rise
N II in uterine arterial blood flow)
• Decreased AT2R expression is associated with preeclamptic
pregnancies
PHASE 4: THE PUERPERIUM
PHASE 4: THE PUERPERIUM

The myometrium remains persistently contracted  compresses large uterine

vessels  prevent haemorrhage

Uterine involution and cervical repair are prompt remodeling processes

Early puerperium  lactogenesis and milk let-down begin in mammary glands

Ovulation generally occurs within 4 to 6 weeks after birth.

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