On average, labor commences 40 ± 2 weeks following
the last menstrual period. The factors involved in the initiation
of labor are as yet not entirely elucidated but likely involve overdistention
of the uterus, enhanced myometrial sensitivity to oxytocin, and
altered prostaglandin synthesis by fetal membranes and decidual
tissues. Although circulating oxytocin levels often do not increase
at the beginning of labor, the number of myometrial oxytocin receptors
rapidly increases. Several prodromal events also usually precede
true labor about 2–4 weeks prior to delivery: the fetal
presenting part settles into the pelvis (lightening); patients develop
uterine (Braxton Hicks) contractions that are characteristically
irregular in frequency, duration, and intensity; and the cervix
softens and thins out (cervical effacement). Approximately 1 week
to 1 h before true labor, the cervical mucous plug (which is often
bloody) breaks free (bloody show).
True labor begins when the sporadic and haphazard Braxton Hicks
contractions increase in strength (25–60 mm Hg), coordination,
and frequency (15–20 min apart). Amniotic membranes may
rupture spontaneously prior or subsequent to the onset of true labor.
Following progressive cervical dilatation, the contractions propel
first the fetus and then the placenta through the pelvis and perineum.
By convention, labor is divided into three stages. The first stage
is defined by the onset of true labor and ends with complete cervical
dilatation. The second stage begins with full cervical dilatation,
is characterized by fetal descent, and ends with complete delivery
of the fetus. Finally, the third stage extends from the birth of
the baby to the delivery of the placenta.
Based on the rate of cervical dilatation, the first stage is
further divided into a slow latent phase followed by a faster active
phase (Figure 42–3). The latent
phase is characterized by progressive cervical effacement and minor
dilatation (2–4 cm). The subsequent active phase is characterized
by more frequent contractions (3–5 min apart) and progressive
cervical dilatation up to 10 cm. The first stage usually lasts 8–12
h in nulliparous patients and about 5–8 h in multiparous
Contractions during the second stage occur 1.5–2 min
apart and last 1–1.5 min. Although contraction intensity
does not appreciably change, the parturient, by bearing down, can
greatly augment intrauterine pressure and facilitate expulsion of
the fetus. The second stage usually lasts 15–120 min and
the third stage typically 15–30 min.
The course of labor is monitored by uterine activity, cervical
dilatation, and fetal descent. Uterine activity refers to the frequency
and magnitude of uterine contractions. The latter may be measured directly,
with a catheter inserted through the cervix, or indirectly, with
a tocodynamometer applied externally around the abdomen. Cervical
dilatation and fetal descent are assessed by pelvic examination.
Fetal station refers to the level of descent (in centimeters) of
the presenting part relative to the ischial spines (eg, –1
Effect of Labor
on Maternal Physiology
During intense painful contractions, maternal minute ventilation
may increase up to 300%. Oxygen consumption also increases
another 60% above third-trimester values. With excessive
hyperventilation, Paco2 falls
below 20 mm Hg. Marked hypocapnia can cause periods of hypoventilation
and transient maternal and fetal hypoxemia between contractions.
Excessive maternal hyperventilation also reduces uterine blood flow
and promotes fetal acidosis.
Each contraction places an additional burden on
the heart by displacing 300–500 mL of blood from the uterus
into the central circulation (analogous to an autotransfusion).
Cardiac output rises 45% over third-trimester values. The
greatest strain on the heart, however, occurs immediately after
delivery, when intense uterine contraction and involution suddenly
relieve inferior vena caval obstruction and increase cardiac output
as much as 80% above prelabor values.
Effect of Anesthetic
Agents on Uterine Activity & Labor
Halothane, enflurane, isoflurane, sevoflurane, and desflurane
depress uterine activity equally at equipotent doses; all cause
dose-dependent uterine relaxation. Low doses (< 0.75 MAC) of
these agents, however, do not interfere with the effect of oxytocin
on the uterus. Higher doses can result in uterine atony and increase
blood loss at delivery. Nitrous oxide has minimal if any effects.
Opioids minimally decrease the progression of labor, whereas
ketamine in doses < 2 mg/kg appears to have little effect.
Does the use of epidural analgesia for labor increase
the likelihood of a cesarean section or forceps delivery? Older
dogma suggested that regional anesthesia administered early in the
course of labor prolongs it, whereas a regional block given once
labor is well established (eg, 4–5 cm cervical dilation)
has little effect. Recent evidence has cast serious doubts on this
view. Current techniques employing very dilute
combinations of a local anesthetic (eg, bupivacaine 0.125% or
less) and an opioid (eg, fentanyl 5 μg/mL
or less) for epidural or combined spinal–epidural (CSE)
analgesia do not appear to prolong labor or increase the likelihood
of a cesarean section.
The administration of epidural analgesia is normally based on
the patient’s choice. Therefore there is a natural bias
toward epidural analgesia being most often administered to patients
who have maternal or fetal factors that increase the likelihood
of cesarean section or prolong labor (Table 42–2). Moreover, in studies of patients not receiving epidural analgesia, women
who experienced more severe pain (eg, requiring > 50 mg meperidine,
and would have been more likely to request epidural analgesia) had
up to a 10-fold increase in cesarean section rate.
Table 42–2. Factors That
Prolong Labor, Increase the Likelihood of Cesarean Section, and
Often Cause Patients to Request an Epidural. |Favorite Table|Download (.pdf)
Table 42–2. Factors That
Prolong Labor, Increase the Likelihood of Cesarean Section, and
Often Cause Patients to Request an Epidural.
|High parenteral analgesic requirements|
|Use of oxytocin|
The specific effects of regional anesthesia are complex and predominantly
indirect. Direct effects are observed only with toxic systemic levels
of local anesthetics, producing tetanic contractions. Indirect effects
mostly relate to local anesthetic and opioid concentrations, intravenous
fluid boluses, and the use of epinephrine. In the past, when higher
concentrations of local anesthetic (eg, bupivacaine 0.25%)
were used, regional anesthesia increased the incidence of low forceps deliveries.
Intense regional analgesia/anesthesia can remove the urge
to bear down during the second stage (Ferguson reflex) and motor
weakness can impair expulsive efforts, often prolonging the second
stage of delivery. Use of dilute local anesthetic/opioid
mixtures (see Chapter 43) can preserve motor
function and allows more effective pushing. Intravenous fluid loading
(crystalloid boluses) is often use to prevent or reduce the severity
of hypotension following an epidural injection. This practice has
been shown to reduce endogenous oxytocin secretion from the pituitary
and can transiently decrease uterine activity. Epinephrine-containing
local anesthetic solutions can theoretically prolong the first stage
of labor if absorption of epinephrine from the epidural space
results in significant systemic β-adrenergic effects.
Although somewhat controversial, prolongation of labor is generally
not clinically observed with very dilute (eg, 1:400,000) epinephrine-containing
Uterine muscle has both α- and β-receptors. α1-Receptor
stimulation causes uterine contraction, whereas β2-receptor
stimulation produces relaxation. Large doses of α-adrenergic
agents, such as metaraminol and phenylephrine, in addition to causing
uterine arterial constriction, can produce tetanic uterine contractions.
Small doses of phenylephrine (50 μg) may increase
uterine blood flow in normal parturients by raising arterial blood
pressure. In contrast, ephedrine has little effect on uterine contractions.
Oxytocin (Pitocin) is usually administered intravenously to induce
or augment uterine contractions or to maintain uterine tone postpartum.
It has a half-life of 3–5 min. Induction doses for labor
are 0.5–8 mU/min. Complications
include fetal distress due to hyperstimulation, uterine tetany,
and, less commonly, maternal water intoxication. Rapid intravenous
infusion can also cause transient systemic hypotension due to relaxation
of vascular smooth muscle; reflex tachycardia may also be noted.
Methylergonovine (Methergine) causes intense and prolonged uterine
contractions. It is therefore given only after delivery (postpartum)
to treat uterine atony. Moreover, because it also constricts vascular
smooth muscle and can cause severe hypertension, it is usually administered
only as a single 0.2 mg dose intramuscularly.
Carboprost tromethamine (Hemabate) is a synthetic analogue of
prostaglandin F2 that stimulates uterine contractions.
It is often used to treat refractory postpartum hemorrhage. As with
methergine, it should be administered only intramuscularly. An initial
dose of 0.25 mg may be repeated every 15–90 min to a maximum
of 2 mg. Common side effects include nausea, vomiting, and diarrhea.
Magnesium is used in obstetrics both to stop premature labor
(tocolysis) and to prevent eclamptic seizures (see Chapter
43). It is usually administered as a 4 g intravenous loading
dose (over 20 min) followed by a 2 g/h infusion.
Therapeutic serum levels are considered to be 6–8 mg/dL.
Serious side effects include hypotension, heart block muscle weakness,
and sedation (see Chapter 28).
The β2-adrenergic agonists ritodrine
and terbutaline inhibit uterine contractions and are used to treat
premature labor (see Chapter 43).