hello and welcome to this aapko basic
00:03
science objective video about the
00:05
physiology of labour the objectives of
00:07
this video are define the four phases of
00:10
parturition and how they correlate to
00:12
the stages of labour describe the
00:14
regulation of uterine activity in
00:16
pregnancy deconstruct the maternal and
00:18
fetal signaling that initiate labour and
00:20
explain the role of oxytocin in the
00:23
regulation of labour and stimulation of
00:25
smooth muscle activity
00:27
Hany medical students a Curie how are
00:29
you doing great I’m just reviewing labor
00:32
I finished the app give IDEO Zhan
00:34
intrapartum care and labour abnormality
00:36
so that was really helpful
00:38
I even reviewed the Freeman curve so I’m
00:40
ready for sign out that is great but you
00:43
know there are some changes to the way
00:44
we think of labour see Freeman’s curve
00:47
had people moving very quickly after
00:49
four centimeters and he thought this is
00:51
when you entered the active phase of
00:53
labour
00:53
however the consortium on safe birth
00:56
took a look at more recent data on
00:57
labour and found that women progress
00:59
much slower from four to six centimeters
01:01
than previously considered especially in
01:04
nulliparous women this has really helped
01:07
us change our definition of labour
01:09
dystocia as well as failed labour here’s
01:12
the paper citation so you can look at it
01:14
before you sign out that’s great thanks
01:16
so much but just one more question what
01:19
actually starts labour as in what is the
01:23
mechanism that allows some women to
01:25
deliver a term and others preterm whoa
01:29
ho that is heavy but you know doctor
01:32
knows all is on I bet he will know the
01:34
answer
01:36
suit I hear you seek knowledge of labour
01:40
this is a topic deep in basic science
01:44
understanding now turn on the crystal
01:47
screen of knowledge then let’s get
01:49
started
01:51
here young doctors this is uh dr. nose
01:59
all uh uh I don’t understand maybe a
02:03
little clarification I see let’s take it
02:07
one step at a time young doctor now
02:10
listen the uterine muscle is active
02:13
throughout the phases of parturition
02:15
during phase one quiescence the uterine
02:19
smooth muscle relaxants with maintenance
02:21
of cervical structural integrity
02:23
inherent myometrium contractility is
02:26
suspended the uterine muscle is
02:30
primarily unresponsive to stimuli this
02:33
is the prelude to parturition and occurs
02:36
from conception to the initiation of
02:38
part Jewish phase two of part revision
02:42
is activation this phase lasts until the
02:45
onset of labor it is marked by cervical
02:48
extracellular matrix changes that leads
02:51
to increased tissue compliance otherwise
02:54
known as cervical softening this
02:56
softening is the result of increased
02:58
vascularity stromal hypertrophy
03:01
glandular hypertrophy and progressive
03:04
structural changes to the extracellular
03:06
matrix cervical collagen undergoes
03:09
conformational changes in the covalent
03:12
cross-links between proteins that alter
03:14
tissue strength and flexibility there
03:17
are many factors associated with
03:19
maintaining and then moving from phase 1
03:21
to phase 2 however much is unknown about
03:25
the role of the fetus in these phases or
03:28
how to manipulate these factors to
03:30
prevent pathology such as cervical
03:32
insufficiency increased prostaglandin
03:35
synthesis in the uterus increased gap
03:37
Junction formation in the myometrium and
03:39
up regulation of oxytocin receptors all
03:42
occur during phase 2 partition
03:45
progesterone and PG also affect two
03:49
cervical ripening causing a breakdown of
03:51
stromal elements that allows for the
03:53
effacement and dilation and phase one
03:55
and two of our tuition
03:57
phase three the stimulation phase begins
04:01
with the onset of labor and ends with
04:04
delivery labor at term is a
04:07
multifactorial event with changes in
04:09
myometrium decidua and cervix over days
04:13
and weeks the initial trigger for labor
04:17
at term is thought to be activation of
04:20
the fetal hypothalamic pituitary access
04:23
the fetal HPA access produces ACTH and
04:27
the placenta produces
04:29
corticotropin-releasing hormone or CRH
04:32
which act on the fetal adrenal glands to
04:35
release production of DHT a s
04:38
DHEA s is then converted in the placenta
04:42
to estriol
04:43
and estradiol estriol enhances maternal
04:47
decidua transcription of p GF 2 alpha
04:50
prostaglandin or PG and oxytocin
04:54
receptors and gap Junction formation in
04:56
the myometrium during phase 3
05:00
stimulation endocrine autocrine and
05:03
paracrine factors from the Phaedo
05:06
placental unit transform irregular
05:08
contractions to regular contractions
05:12
phase 3 is one of the most complex
05:14
phases and pathology here can lead to
05:17
preterm labor labor dystocia and post
05:20
turn pregnancies in non-human mammals we
05:24
know that the fetus has a central role
05:25
to play in initiating this cascade
05:28
however in humans this role is not well
05:31
understood in theory the mediators we
05:34
discussed previously fetal cortisol DHEA
05:38
s placental estriol
05:40
oxytocin prostaglandin and c rh may
05:43
alter their receptor frequency during
05:45
phase 3 to initiate and complete labor
05:48
more research is needed to understand
05:51
the precise mechanism of human
05:53
parturition let’s pause they can apply
05:58
which one of these mediators of labor do
06:00
we already manipulate in an attempt to
06:02
prevent recurrent preterm labor studies
06:05
have demonstrated that weekly injection
06:07
a 250 milligrams of 17 hydroxy
06:10
progesterone caraway from 16 to 36 weeks
06:13
of gestation reduces the risk of
06:15
recurrent preterm delivery
06:16
it appears the progesterone is important
06:19
in maintaining uterine quiescence in the
06:22
third trimester by limiting the
06:23
production of stimulating prostaglandins
06:25
and inhibiting the expression of genes
06:27
regulating formation of oxytocin and
06:30
prostaglandin receptors and gap
06:32
junctions in the myometrium labor is
06:35
associated with a functional withdrawal
06:37
a progesterone activity in the uterus oh
06:40
wow but wait sir you said there were
06:44
four stages of partition but it seems
06:46
like stage 3 was the end what could be
06:48
left you are right to remember stage 4
06:52
and it should not be trivialized it
06:55
involves uterine involution and return
06:58
to pre pregnancy physiology and Anatomy
07:01
this is essential for maternal survival
07:04
and is mediated by oxytocin recall that
07:08
oxytocin is a peptide hormone that is
07:10
synthesized in the hypothalamus and then
07:13
secreted in a pulsatile fashion from the
07:16
posterior pituitary and interestingly
07:19
the decidua extraembryonic and placental
07:22
fetal tissue as well oxytocin stimulates
07:26
smooth muscle uterine contractions
07:28
receptor expression is increased nearly
07:31
200 fold
07:32
during the second phase of parturition
07:34
or the activation phase more receptors
07:38
are located in the fundus of the uterus
07:40
compared to the lower uterine segment
07:43
oxytocin activates phospholipase C which
07:47
increases intracellular calcium these
07:50
increased calcium levels stimulate the
07:52
calmodulin mediated activation of myosin
07:55
light-chain kinase to affect uterine
07:58
smooth muscle contraction
08:00
and remember medical student Zachary we
08:03
can give oxytocin exogenously and labor
08:05
and postpartum to further stimulate
08:08
uterine contractions and thus overcoming
08:10
dysfunctional labor or uterine atony it
08:12
is important to know if we are on
08:14
menteng labor with oxytocin that the
08:16
biologic half-life of oxytocin is only
08:19
three to four minutes while the
08:20
circulatory half-life can be 10 to 12
08:23
minutes and even more striking the
08:25
uterine effects can last as long as 20
08:27
to 40 minutes you have learned much
08:31
already young doctor medical student
08:34
Zachary have we filled your thirst for
08:36
knowledge today yes but no sir I still
08:41
want to know exactly why labor starts in
08:42
some women and not others but at least I
08:45
now know what mediators to consider as I
08:47
start my own research quest
08:49
[Music]
08:51
this concludes this aapko basic science
08:53
objective video about the physiology of
08:55
labor you should be able to define the
08:58
four phases of parturition and how they
09:00
correlate to the stages of labor
09:02
describe the regulation of uterine
09:04
activity in pregnancy deconstruct the
09:07
maternal and fetal signaling that
09:08
initiate labor and explain the role of
09:10
oxytocin in the regulation of labor and
09:13
stimulation of smooth muscle activity
09:17
namaste and thanks for watching
09:24
[Music]
09:30
[Music]
09:33
you
09:36
[Music]
09:43
you
09:44
[Music]

00:00
labor is the most ordinary thing you’ll
00:02
ever do and also the most extraordinary
00:10
hey guys today is June 14th and tomorrow
00:15
I am scheduled for an induction of this
00:18
baby we said goodbye to Carson tonight
00:20
he went with my mom he’s having a little
00:22
sleepover and just facing some things
00:24
that they saw in the ultrasound and the
00:25
fact I’m almost 42 weeks pregnant this
00:28
baby needs to come out so we’re doing a
00:30
last-ditch effort to start labor tonight
00:32
and we’re gonna get some Mexican food
00:35
it’s like so good Charlie got a plastic
00:39
quesadilla races well it’s got crabs
00:41
that’s not last so its induction day
00:45
June 15th around 7 a.m. or so and I got
00:49
a call at 5:30 this morning from the
00:51
doctor’s office saying that every single
00:54
hospital bed is full and they need to
00:56
postpone my induction what’s even
00:59
crazier is that my contractions started
01:01
this morning at like 4:00 4:30 and
01:05
they’ve been coming every like 10 to 20
01:07
minutes which is absolutely insane it’s
01:10
good it’s good it’s just it’s just so
01:12
crazy how this is panning out hey so I
01:17
don’t usually do these but we’re just
01:19
about getting ready to head out to the
01:21
hospital um just clean up around here
01:24
and Katherine’s getting ready so here we
01:26
go back in the car
01:28
and we are headed to the hospital right
01:30
now there are beds free my contractions
01:33
basically completely stopped so they’re
01:35
going to take a look at things and we’re
01:36
gonna see where we are
01:42
yeah new patient checking names so
01:54
glamorous
02:02
finally in book ten waiting for the
02:04
doctor to come I’ll hook it up his
02:07
little heartbeats going over there and
02:09
I’ve had one contraction since being
02:10
here so it’s a really really good sign
02:16
water was broken maybe fifteen or twenty
02:18
minutes ago and it’s already doing some
02:22
heavier contractions doing great
02:31
are you doing you’re beautiful
02:36
Thanks just when they break your water
02:39
like you forget how much it hurts and it
02:42
makes it hurt a little more because
02:44
there’s no cushion so you feel like this
02:46
like oh that plum
02:50
it’s about 12:30 middle and we are
02:53
really in it comes with good
02:55
contractions Catherine is God he’s hurt
02:59
really bad he’s hanging in there she’s a
03:03
trooper she’s doing great
03:16
Oh
04:00
the year has gone so on your birthday
04:07
back right drumroll said let me reveal 9
04:17
pounds 8 ounces hey boy
04:40
it’s your birthday
04:43
I wanted to check in with everyone a
04:47
winds here he’s doing great
04:50
Katherine’s doing great too and we’re
04:52
just so happy and boots on the way this
05:02
is a really pretty closet my mom got me
05:04
with two hearts on it to represent the
05:06
two sweet daddy’s catching some Z’s on
05:14
this awesome chair how was the night we
05:18
sucked like what the two hours but it’s
05:22
okay we’re doing really good just about
05:24
to some breakfast food
05:46
oh did you get to be aa ring me back
05:54
clean that screen but the desert anyone
05:57
loves it we have to guess what is granny
06:21
get ready to hatch down hungry kid
06:30
always hungry oh well
06:37
every step that we take as one
06:43
all
06:48
our love
06:53
our love well
06:57
Oh

Electronic fetal monitors continuously record the instantaneous fetal heart rate on the upper channel and uterine contractions on the lower channel. They do this by attaching, either externally (and non-invasively) or internally, to detect the fetal heart and each uterine contraction.

Labor is an inherently dangerous life event for a fetus and its mother. In the majority of cases, everything goes smoothly enough and ends happily. In a minority of cases, there are some problems. Electronic fetal monitoring is used to provide:
1. Minute-by-minute information on the status of the fetus
2. Accurate historical information on fetal status and the frequency/duration of contractions from earlier in labor.
3. Insight into the stresses on the fetus and its ability to tolerate those stresses.

Originally, electronic fetal monitoring was thought to be able to prevent such newborn problems as stillbirth, brain damage, and cerebral palsy. This hope proved to be overly optimistic. Unfortunately, and contrary to earlier thinking, most of the problems that lead to stillbirth, brain damage, and cerebral palsy are not intrapartum problems, but have already occurred by the time a patient comes in to labor and delivery.

Nonetheless, electronic fetal monitoring has proved so useful in so many ways that it has become a prominent feature of intrapartum care, and indispensable for high risk patients.

Two forms of continuous electronic fetal heart monitoring are used, internal and external.
• Internal monitoring provides the most accurate information, but requires a scalp electrode be attached to the fetus, and a pressure-sensing catheter to be inserted inside the uterine cavity. Both of these require membranes be ruptured and both have small, but not inconsequential risks. For that reason, they are usually used only when the clinical circumstances justify the small increased risk of complication.
• External monitoring usually provides very good information about the timing of contractions and the fetal response. External monitoring consists of belts worn by the mother during labor that record the abdominal tension (indirectly recording a contraction), and the instantaneous fetal heart rate. External monitoring has the advantages of simplicity, safety, availability, and reasonable reliability under most general obstetrical circumstances. However, it is subject to more artifact than internal monitoring, may not detect subtle changes, and may not accurately record the information, particularly if the mother is overweight or active.

Uterine Blood Flow

Maternal blood flows to the uterus primarily through the uterine arteries. The arteries branch out, once they enter the uterus, and supply blood to the muscle cells of the myometrium, and through the wall to the intervillous space (IVS). Once the maternal blood reaches the IVS, it simply dumped into the space, where it drifts about until some is drained off through the maternal venous system. Unlike the highly controlled capillary circulation, there is little control over this process. The intervillus space is similar to a swimming pool, where fresh water is dumped in through a faucet (the maternal arterioles), while the drains in the bottom of the pool (maternal venous system) sucks up any available water that happens to be nearby.

The placenta floats on top of the IVS, with its chorionic villi dipping down into the pool. Across the villous membrane pass oxygen, carbon dioxide, nutrients and waste products. Some of this passage is active transport (eg, glucose), some facilitated (eg, because of pH gradient), and some is passive.

Many factors influence uterine blood flow delivery to the IVS, including:
• Maternal position (lateral, recumbant improves flow)
• Maternal exercise (decreases flow)
• Surface area of the placenta (placental abruption decreases flow)
• Hypotension or hypertension (both decrease flow)
• Uterine contractions (contractions reduce flow)

Once the maternal blood reaches the IVS, oxygen and nutrients must still must traverse the villous membrane. If thickened (as with edema or infection), then transvillous transport of materials will be impaired, at least to some degree.

Baseline Fetal Heart Rate

The baseline fetal heart rate is normally between 110 and 160 beats per minute. This seems to be the range that the normal, healthy fetus prefers to keep itself well-supplied with oxygen and nutrients. The heart can beat faster, but only at a cost of increased energy utilization that is normally not justified. The heart can beat slower, but if the bradycardia is prolonged, it can lead to progressive tissue oxygen debt.

Tachycardia

Tachycardia is the sustained elevation of fetal heart rate baseline above a 160 BPM. Tachycardia can be a normal response to some increased need for oxygen, for example:
• Increased fetal activity (everyone’s heart rate goes up when we exercise)
• Maternal fever (with an elevated body temperature, all enzyme systems speed up, increasing the need for oxygen on a metabolic basis)

It can also increase in the presence of more worrisome problems, including:
• Chorioamnionitis
• Maternal hypothyroidism
• Drugs (tocolytics, Vistaril, etc.)
• Fetal hypoxia
• Fetal anemia
• Fetal heart failure
• Fetal arrhythmias

Most tachycardias are not indicative of fetal jeopardy, particularly in the absence of any other FHR abnormalities.

Bradycardia

Bradycardia is the sustained depression of fetal heart rate baseline below 110. Most of these are caused by increased vagal tone, although congenital cardiac abnormalities can also be responsible.

Mild bradycardia (to 80 or 90 BPM) with retention of beat-to-beat variability is common during the second stage of labor and not of great concern so long as delivery occurs relatively soon. Moderate to severe bradycardia (below 80 BPM) with loss of beat-to-beat variability, particularly in association with late decelerations, is more troubling and may indicate fetal distress, requiring prompt resolution.

Variability

The normal fetal heart rate baseline is from 110 to 160 BPM and has “variability.” Variability means fluctuations in the fetal heart rate that are irregular in amplitude and frequency.

This variability is further classified by measuring the peak-to-trough distance, in beats per minute.

Absent Variability = No detectable fluctuations
Minimal Variability = Up to 5 BPM fluctuations
Moderate Variability = 6 to 25 BPM fluctuations
Marked Variability = Greater than 25 BPM fluctuations

Variability is normally controlled by the fetal brain through sympathetic and parasympathetic influences. Reduced variability occurs normally during fetal sleep and usually returns after 20 to 40 minutes.
Reduced variability may also occur:
• Following narcotic administration
• With fetal anomalies or injury
• With hypoxia and acidosis in combination with such FHR abnormalities as late decelerations, tachycardia, bradycardia, and severe variable decelerations.

Persistent or progressively reduced variability is not, by itself, a sign of fetal jeopardy. But in combination with other abnormalities may indicate fetal intolerance of labor.

Accelerations

An abrupt increase in fetal heart rate of at least 15 BPM and lasting at least 15 seconds is called an acceleration. These usually occur in response to fetal movement, and can sometimes be provoked by stimulating the fetal scalp during a pelvic examination, or by acoustically stimulating the fetus with a loud, obnoxious noise. The presence of fetal accelerations is a normal findings and indicates the fetus is tolerating the intrauterine environment well.
In pregnancies less than 32 weeks, the height and breadth of fetal accelerations may normally be a little less, at 10 BPM lasting at least 10 seconds.

If the acceleration lasts longer than 2 minutes, then it is classified as a prolonged acceleration. While unusual, it is of no clinical significance. Accelerations lasting longer than 10 minutes are considered a change in fetal heart rate baseline.

Sinusoidal Pattern

This is a smooth, sine-wave like pattern with a wave frequency of 3-5 per minute. By itself, this unusual pattern frequently has no significance, but in combination with a loss of variability is occasionally associated with fetal anemia.

Contraction Patterns

During latent phase labor (prior to 4 cm), contractions may occur every 3-5 minutes and may or may not be painful.

A normal contraction pattern in active labor shows contractions occurring about every 2-3 minutes and lasting about 60 seconds.
• If contractions are less often than every 2-3 minutes in the active phase, labor may progress more slowly, if at all. While less frequent contractions are the rule in latent phase labor (prior to 4 cm), they are the exception in active labor.

Coupling

Coupling means that two contractions occur one right after the other rather than the normal pattern. Usually, coupling is followed by a longer contraction-free interval. Tripling can also be seen where three contractions occur without any significant recovery time.

If labor is progressing normally, coupling can be ignored. But coupling is often associated with dysfunctional progress in labor. In these cases, coupling can be treated with:
• Rest
• Hydration
• Narcotics
• Epidural Anesthesia
• Oxytocin

Tachysystole

If contractions are persistently more often than 5 contractions in 10 minutes, this is called “tachysystole.” Tachysystole poses a problem for the fetus because it allows very little time for resupply of the fetus with oxygen and removal of waste products. For a normal fetus, tachysystole can usually be tolerated for a while, but if it goes on long enough, the fetus can be expected to become increasingly hypoxic and acidotic.

Tachysystole is most often caused by too much oxytocin stimulation. In these cases, the simplest solution is to reduce or stop the oxytocin to achieve a more normal and better tolerated labor pattern. Other causes of tachysystole include:
• Dehydration
• Placental abruption
• Pre-eclampsia
• Amnionitis

In cases of spontaneous tachysystole, increasing maternal hydration and placement in the lateral decubitus position may slow the contractions.

Effect of Contractions

The placenta floats on a lake of blood, called the intervillus space. This lake contains several hundred cc’s of maternal blood at full term. The blood is deposited in the lake by open maternal arteries, and is drained from the lake by open maternal veins. There is no capillary flow on the maternal side.
The placenta, floating on the lake, has finger-like projections, called villi that dip down into the lake. Fetal capillary circulation passes through these villi, and this is where gas, nutrient, and waste exchange between the mother and baby occurs.

During a uterine contraction, blood flow through the uterus slows, because the maternal vessels are being compressed by the myometrium. If the contraction is strong enough, all blood flow through it will stop.

Maternal mean arterial pressure (MAP) is around 85 mm Hg. The pressure on the inside of the uterus (at rest) is around 10 mm Hg. The pressure within the uterine muscle (intramyometrial pressure or IMP) is usually about 2-3 times that of the intra-amniotic pressure. Because of these pressures, blood flows from the high pressure uterine arteries, through the intramyometrial spiral arteries (and past the medium pressure intramyometrial zone) and into the low pressure intravillous space. From the IVS, blood is drained out through the even lower pressure venous system and returned to the mother’s circulation.
During a contraction, the intramyometrial pressures rise with the increased muscle tone. As the compressive pressure rises, blood flow through the spiral arteries diminishes (less pressure gradient to drive the blood through them), and then stops when the IMP equals the MAP. The IMP usually equals the MAP when the amniotic fluid pressure is around 40 mm Hg. (Remember that the intramyometrial pressure is 2-3 time that of the amniotic fluid pressure).

As the contraction eases up, blood flow through the spiral arteries resumes and by the end of the contraction, blood flow is back to normal.
Thus, with each contraction of any significance, there is initially reduced blood flow to the intervillous space, then a cessastion of blood flow, followed by a gradual resumption of blood flow.

On one level, you could imagine the danger of the fetal oxygen supply being interrupted by each uterine contraction. On another level is the realization that for a normal fetus, this interruption is nearly trivial (similar to holding your breath for 5 seconds). But if the contractions are coming too frequently (with very little time between contractions for the fetus to resupply), or if the fetus already has a significant problem, then contractions can pose a threat.

Periodic Heart Rate Changes

These heart rate changes are recurring throughout labor. They are typically associated in some way with uterine contractions. There are three basic recognized types:
• Early Decelerations
• Late Decelerations
• Variable Decelerations

Each has its own features and clinical significance. In addition, a fetus may demonstrate combined decelerations (for example, a severe variable deceleration with a late deceleration component.)

Early Decelerations

Early decelerations are periodic slowing of the fetal heartbeat, gradual in onset and recovery, and synchronized exactly with the contractions. These dips are rarely more than 20 or 30 BPM below the baseline, but last at least 30 seconds from onset to nadir.

These innocent changes are thought to be due, in many cases, to fetal head compression within the birth canal.

Sometimes, patients demonstrating early decelerations will later develop variable decelerations.

Late decelerations

Late decelerations are repetitive, gradual slowings of the fetal heartbeat toward the end of the contraction cycle. From onset to nadir, they last at least 30 seconds, and have a gradual recovery to the baseline. They are felt to represent some degree of utero-placental insufficiency.
All blood flow in and out of the IVS stops briefly during a contraction. A normal fetus with normal reserve (oxygen in its bloodstream, in the blood of the placenta, and in the intravillous space) will probably not notice the tiny drop in total oxygen availability during these contractions. But a fetus who has used up its reserve, or cannot maintain its reserve will, over the course of the contraction, develop some degree of hypoxia, hypercarbia and acidosis. This otherwise normal fetus will respond by slowing its heart rate, to conserve energy. The fetal heart is the largest consumer of oxygen in the fetus and if the rate can be slowed, the fetus will survive longer on less oxygen.

After the contraction passes and fresh blood resupplies the intervillous space, the hypoxia, hypercarbia and acidosis is eased and the fetal heart rate returns to normal.

Clinically, the development of late decelerations is a worrisome sign that the fetus has very little reserve. Techniques that may be used to correct this problem include:
• Changing maternal position to improve uterine blood flow
• IV hydration to increase maternal blood volume, presumably leading to increased uterine blood flow
• Administering oxygen to the mother to try to get some additional oxygen through to the fetus. Of the three standard treatments, oxygen administration is the least useful, since the maternal hemoglobin oxygen saturation is likely already 99%. The effect of breathing additional oxygen will probably have minimal effect on the oxygen saturation.
• Decreasing or discontinuing oxytocin infusion to slow down or stop contractions that are provoking the decelerations.
• Tocolytic drugs to slow down or stop contractions that are provoking the decelerations.

If the late decelerations are persistent and non-remediable, this is considered “fetal distress,” “fetal intolerance of labor,” or a “non-reassuring fetal heart rate pattern.” Such patients should be delivered promptly to avoid fetal injury or death. Sometimes cesarean section is required to achieve prompt delivery.
If persistent and not correctable, they represent a threat to fetal well-being.

Variable Decelerations

Variable decelerations are variable in onset, duration and depth. They may occur with contractions or between contractions. They are at least 15 BPM in depth and last at least 15 seconds, but not longer than 2 minutes. Their onset to nadir is less than 30 seconds.

Typically, variable decelerations have an abrupt onset and rapid recovery (in contrast to other types of decelerations which gradually slow and gradually recover.

Variable decelerations are thought to represent a vagal response to some degree of umbilical cord compression. If the umbilical cord is only slightly compressed, this will obstruct the umbilical vein (low pressure system) which returns re-oxygenated blood to the fetal heart. The initial normal fetal response to this is a slight increase in fetal heart rate to compensate for the lack of blood return and the slowly diminishing oxygen supplies. If this slight increase in FHR is followed by a major drop in FHR, this phenomenon is called a “shoulder.”

As pressure on the umbilical cord increases, the high-pressure umbilical arteries become occluded. When this happens, there is an immediate rise in fetal blood pressure. 30% of the fetal cardiac output goes to the placenta and if that flow is blocked, the fetus will rapidly develop significant hypertension. The normal fetus will respond to this hypertension by immediately slowing the heart down by sending a signal through the vagus nerve. When the umbilical cord obstruction is released, the vagal response disappears and the fetal heart returns to normal.

If a mild degree of cord compression continues (enough to continue to obstruct the umbilical veins for a while), then another “shoulder” may appear at the end of the deceleration.

If the variable deceleration lasts long enough to cause hypoxia, there may be a more gradual rise back to the baseline and some “overshoot.” Overshoot means the heart rate goes higher than the baseline for a while, to compensate for the mild degree of hypoxia and acidosis that has occurred during that deceleration. If you exercise vigorously for a minute, your muscle tissues will acquire some degree of oxygen debt and a mild degree of local acidosis. When you sit down and rest, your heart rate will be higher than before you started exercising, but will return to normal as you resupply your muscles with oxygen and remove the local waste products. The fetus responds in a similar fashion.
Variable decelerations, unlike late decelerations, are not caused by hypoxia, although if severe enough, frequent enough and persistent enough, can ultimately lead to some degree of fetal acidosis.

The interventions to effectively treat variable decelerations may include:
• Changing maternal position to improve uterine blood flow
• IV hydration to increase maternal blood volume, presumably leading to increased uterine blood flow
• Administering oxygen to the mother to try to get some additional oxygen through to the fetus. Of the three standard treatments, oxygen administration is the least useful, since the maternal hemoglobin oxygen saturation is likely already 99%. The effect of breathing additional oxygen will probably have minimal effect on the oxygen saturation.
• Amnioinfusion to improve oligohydramnios
• Decreasing or discontinuing oxytocin infusion to slow down or stop contractions that are provoking the decelerations.
• Tocolytic drugs to slow down or stop contractions that are provoking the decelerations.
• Digital elevation of the fetal head out of the maternal pelvis to ease pressure on the umbilical cord.

Occasional mild or moderate variable decelerations are common and not considered threatening. They are seen in the majority of laboring patients at some time or other. They are more common in the second stage of labor.
Mild variable decelerations do not dip below 70 BPM and last less than 30 seconds.

Severe variable decelerations dip below 60 BPM for at least 60 seconds (“60 x 60”). If persistent and not correctable by simple means, they can be threatening to fetal well-being. Like persistent, non-remediable late decelerations, fetuses demonstrating persistent, non-remediable severe variable decelerations should be delivered promptly, preferably vaginally, but by cesarean section if necessary.

Prolonged decelerations

Prolonged decelerations last more than 2 minutes and occur in isolation. Causes include maternal supine hypotension, epidural anesthesia, paracervical block, tetanic contractions, and umbilical cord prolapse.
Some of these are largely self-correcting, such as the deceleration following paracervical block, while others (maternal supine hypotension) respond to simple measures such as repositioning.

Other causes (such as umbilical cord prolapse) require prompt intervention to avoid or reduce the risk of fetal injury.

EFM Categories

In 2008, the National Institute of Child Health and Human Development issued a statement with recommended categories for describing EFM tracings.
• Category I means normal, with a baseline between 110 and 160, moderate variability, and no late or variable decelerations.
• Category II means not Category I or III, and is indeterminate in its significance.
• Category III means abnormal, with absent variability, accompanied by bradycardia, or variable decelerations, or late decelerations, or a sinusoidal pattern.

Describing a Tracing

In communicating the pattern seen on an electronic fetal monitor tracing, it is useful to use a systematic approach, primarily to avoid omitting important information. I recommend you use this 4-step approach.
1. Contractions. Start with the contraction pattern. In this example, I would say, “There are regular uterine contractions every 2-3 minutes, lasting 60 seconds.”
2. Baseline. Next, provide the baseline fetal heart rate and variability. In this case, I would say, “The baseline fetal heart rate is 140 BPM and has moderate variability.”
3. Decel/Accel. Next, describe accelerations and decelerations. In this tracing, I would say, “There are multiple fetal accelerations greater than 15 x 15, and no decelerations.
4. Category. Last, Categorize the tracing as Category I, II, or III. “This is a Category I tracing.”

Variable deceleration are no longer described as mild, moderate and severe.

For an excellent overview of intrapartum fetal heart rate monitoring, please review ACOG practice bulletin 106

https://www.acog.org/clinical/clinical-guidance/practice-bulletin/articles/2009/07/intrapartum-fetal-heart-rate-monitoring-nomenclature-interpretation-and-general-management-principles